Analysis of tangential contact boundary value problems using potential functions.

This paper presents an analysis technique of high-order contact potential problems and its application to an elastic settlement analysis of a shallow foundation system subjected to a combined traction boundary condition. Closed-form solutions of potential functions are derived for an elastic half-space subjected to bilinear tangential traction boundary conditions over rectangular surface regions. Using the principle of superposition, the present solutions provide a means to form an approximate and continuous solution of elastic contact problems with higher-order tangential boundary conditions. As an application example, an elastic settlement analysis of a rigid footing founded on a dense granular soil is performed under a tangential traction boundary condition prescribed in an analogy with the stress equilibrium states of static sandpiles. A generalized solution approach to combined normal and tangential traction boundary value problems is discussed in the context of foundation engineering.

Application of low-order potential solutions to higher-order vertical traction boundary problems in an elastic half-space.

New solutions of potential functions for the bilinear vertical traction boundary condition are derived and presented. The discretization and interpolation of higher-order tractions and the superposition of the bilinear solutions provide a method of forming approximate and continuous solutions for the equilibrium state of a homogeneous and isotropic elastic half-space subjected to arbitrary normal surface tractions. Past experimental measurements of contact pressure distributions in granular media are reviewed in conjunction with the application of the proposed solution method to analysis of elastic settlement in shallow foundations. A numerical example is presented for an empirical 'saddle-shaped' traction distribution at the contact interface between a rigid square footing and a supporting soil medium. Non-dimensional soil resistance is computed as the reciprocal of normalized surface displacements under this empirical traction boundary condition, and the resulting internal stresses are compared to classical solutions to uniform traction boundary conditions.

Changes in the levels of beta-thromboglobulin and inflammatory mediators during extracorporeal membrane oxygenation support.

BACKGROUND: Extracorporeal membrane oxygenation (ECMO) has been associated with platelet dysfunction, but no markers of platelet dysfunction during ECMO have been identified. METHODS: We investigated the potential uses of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) as markers of platelet activation induced by ECMO in vivo. RESULTS: 13 patients who received ECMO for acute respiratory failure were included. Generalized estimating equations were used to examine the associations between days on ECMO and the plasma levels of beta-TG and PF4 and of proinflammatory markers. Analyses were performed before ECMO (baseline) and 24, 48, 72 and 168 hours after the commencement of ECMO. The plasma levels of biomolecules were measured by ELISA and Luminex assay.Percentages of platelets varied widely without statistical significance (p = 0.17). Beta-TG levels significantly decreased over the first 72 hours (p<0.001), but PF4 levels decreased nonsignificantly (p = 0.17). Inflammatory markers, that is, plasma IL-6 (p = 0.03), IL-18 (p<0.001), and MMP-8 (p<0.01) levels stabilized during an early period of ECMO support. CONCLUSIONS: Our data suggest that ECMO use may not affect platelet activation during the first 3 days of ECMO. Plasma beta-TG levels may allow assessment of the time-dependent extent of ECMO-induced platelet dysfunction in patients with acute respiratory failure.

Diffuse sclerosing variant of papillary thyroid carcinoma: major genetic alterations and prognostic implications.

AIM: Diffuse sclerosing variant of papillary thyroid carcinoma (DSV-PTC) is an uncommon variant of PTC, and its prognostic significance remains controversial. The aim of this study was to investigate the major genetic alterations of DSV-PTC and their prognostic implications. METHODS AND RESULTS: We included 37 patients with DSV-PTC who underwent thyroid surgery and had formalin-fixed paraffin-embedded samples. We tested for a panel of genetic alterations, including BRAF(V) (600E) , NRAS codon 61, HRAS codon 12/13/61 and KRAS codon 12/13 point mutations as well as RET/PTC1, RET/PTC3 and PAX8/PPARγ rearrangements using reverse transcription real-time polymerase chain reaction (PCR). All genetic alterations found on PCR were confirmed by Sanger sequencing. Associations between the identified genetic alterations and clinicopathological characteristics were evaluated. Among 37 cases of DSV-PTC, 17 were positive for RET/PTC1 (46%), six for RET/PTC3 (16%) and nine for BRAF(V) (600E) (24%). All mutations/rearrangements were mutually exclusive. The remaining five cases had none of the above genetic alterations. DSV-PTC with RET/PTC3 rearrangement was associated with advanced-stage disease, including T4 and distant metastasis (P < 0.05). Patients with RET/PTC3 showed a higher frequency of persistent disease (P < 0.01). In contrast, DSV-PTC with RET/PTC1 was associated with a higher prevalence of disease remission (P < 0.05) and coexistent Hashimoto's thyroiditis (P < 0.01). CONCLUSION: Taken together, RET/PTC rearrangement was the major genetic alteration seen in patients with DSV-PTC, and the RET/PTC3 rearrangement was associated with advanced stage at diagnosis and poor clinical outcome.

Upregulation of endothelial adhesion molecules by lysophosphatidylcholine. Involvement of G protein-coupled receptor GPR4.

Lysophosphatidylcholine induces expression of adhesion molecules; however, the underlying molecular mechanisms of this are not well elucidated. In this study, the intracellular signaling by which lysophosphatidylcholine upregulates vascular cell adhesion molecule-1 and P-selectin was delineated using YPEN-1 and HEK293T cells. The results showed that lysophosphatidylcholine dose-dependently induced expression of vascular cell adhesion molecule-1 and P-selectin, accompanied by the activation of transcription factor nuclear factor kappaB. However, the nuclear factor kappaB inhibitor caffeic acid phenethyl ester (CAPE) and the antioxidant N-acetylcysteine only partially blocked lysophosphatidylcholine-induced adhesion molecules. Subsequently, we found that the lysophosphatidylcholine receptor G protein-coupled receptor 4 (GPK4) was expressed in YPEN-1 cells and triggered the cAMP/protein kinase A/cAMP response element-binding protein pathway, resulting in upregulation of adhesion molecules. Further evidence showed that overexpression of human GPK4 enhanced lysophosphatidylcholine-induced expression of adhesion molecules in YPEN-1 cells, and enabled HEK293T cells to express adhesion molecules in response to lysophosphatidylcholine. In conclusion, the current study suggested two pathways by which lysophosphatidylcholine regulates the expression of adhesion molecules, the lysophosphatidylcholine/nuclear factor-kappaB/adhesion molecule and lysophosphatidylcholine/GPK4/cAMP/protein kinase A/cAMP response element-binding protein/adhesion molecule pathways, emphasizing the importance of the lysophosphatidylcholine receptor in regulating endothelial cell function.

Pulmonary involvement in Erdheim-Chester disease.

Erdheim-Chester disease is a disseminated non-Langerhans' cell histiocytosis involving multiple organs with characteristic sclerotic musculoskeletal lesions. This is the report of the case of a 53-year-old woman with extensive and progressive pulmonary disease. Computed tomography scans revealed diffuse infiltrative lung disease. Thoracoscopic lung biopsy and a biopsy of the right femur lesion were performed. The histopathology revealed that she had non-Langerhans' cell histiocytosis; Erdheim-Chester disease. The characteristic lesions of Erdheim-Chester disease, including involvement of the orbit, pericardium, periaorta, and bone were detected. This helped to further confirm that the patient had Erdheim-Chester disease with associated pulmonary involvement. As Erdheim-Chester disease is a rare non-Langerhans' cell histiocytosis that may be misdiagnosed as interstitial lung disease or other pulmonary disorders, this diagnosis should be considered in the differential diagnosis of such lung lesions.