Thymic cancer in lynch syndrome: an unusual association.

Lynch syndrome has been associated with predominantly colorectal, endometrial, and ovarian cancer. We report hereby an unusual case of thymic carcinoma in a patient with Lynch syndrome. A 45-year-old Caucasian woman with a personal history of Lynch syndrome (MLH1 heterozygous mutation) presented with dyspnea, chest pain, and dysphagia.

A left knee wound complication by non-Hodgkins lymphoma in bilateral total knee arthroplasties.

A 70-year-old woman with a history of bilateral primary knee osteoarthritis presented with a left knee wound complication, a non-Hodgkins lymphoma, after bilateral total knee arthroplasties. After exploring several etiologies, the evidence in this unusual case suggests a coincidental preexisting lymphoma.

Inflammation-induced subcellular redistribution of VE-cadherin, actin, and gamma-catenin in cultured human lung microvessel endothelial cells.

The inflammation-induced subcellular redistribution of key cytoskeletal and junctional proteins in cultured human lung microvessel endothelial cells is investigated as part of a study on the posttranslational regulation of paracellular permeability. Inflammatory agonist-stimulated cells are detergent fractionated into three subcellular compartments followed by quantitative immunoblot analysis. Actin, gamma-catenin, and VE-cadherin increasingly associate with the cytoskeletal fraction upon thrombin stimulation.

Changes in the biomechanical properties of neutrophils and endothelial cells during adhesion.

This study examined changes in the biomechanical properties of cultured pulmonary microvascular endothelial cells (ECs) and neutrophils induced by adhesion of neutrophils to these ECs. The biomechanical properties of cells were evaluated using magnetic twisting cytometry, which measures the angular rotation of ferromagnetic beads bound to cells through antibody ligation on application of a specified magnetic torque. Adhesion of neutrophils to 24-hour tumor necrosis factor-alpha (TNF-alpha)-treated ECs, but not to untreated ECs, induced an increase in EC stiffness within 2 minutes, which was accompanied by an increase and a reorganization of F-actin in ECs.

NFkappaB translocation in human microvessel endothelial cells using a four-compartment subcellular protein redistribution assay.

Protein distribution profiles may be used to characterize both physiological and pathophysiological cellular changes, but rigorous biochemical assays for measuring such movements are lacking. This paper reports on a protein redistribution assay that combines reversible metal chelate-based total protein detection with a four-fraction subcellular detergent fractionation procedure. TNF-alpha stimulated cultured human omental microvessel endothelial cells are fractionated into cytosol, membrane/organelle, nuclear (envelope and associated), and cytoskeletal/DNA compartments.

Soluble P-selectin moderates complement-dependent reperfusion injury of ischemic skeletal muscle.

P-selectin is an adhesion molecule expressed on activated endothelial and platelet surfaces. The function of the short consensus repeats (SCRs) of P-selectin, homologous with the SCRs of complement regulatory proteins is largely unknown. In a model of murine hindlimb ischemia where local reperfusion injury is partly mediated by IgM natural antibody and classical complement pathway activation, we hypothesized that human soluble P-selectin (sP-sel) would moderate the complement component of the inflammatory response.

Comparative effects of garlic and aspirin on diabetic cardiovascular complications.

By using streptozotocin-induced diabetic rats as a studied model, our previous experimental results have indicated that daily oral feeding of garlic extract (100 mg/kg BW) could increase the cardiovascular functions in streptozotocin (STZ) rats; the abnormality of lipid profile was prevented; and garlic extract could increase fibrinolitic activities with the decrease of platelet aggregation. Moreover, the plasma insulin level was increased concomitantly with the decrease of plasma glucose level. However, due to the high incidence of atherosclerosis in diabetes, the present study has been continued for further investigation of the effect of garlic extract on the coronary vascular ultrastructural changes.

Myosin translocation in retinal pericytes during free-radical induced apoptosis.

Vascular pathologies induced by ischemia/reperfusion involve the production of reactive oxygen species (ROS) that in part cause tissue injury. The production of ROS that occurs upon reperfusion activates specific second messenger pathways. In diabetic retinopathy there is a characteristic loss of the microvascular pericyte.

Selective propagation of retinal pericytes in mixed microvascular cell cultures using L-leucine-methyl ester.

Endothelial cell (EC) propagation has been simplified by developing cell-specific selection criteria. Methods commonly used for selectively isolating EC include: (i) differential sieving of disaggregated tissue, (ii) differential plating of cells on extracellular matrices, (iii) lectin affinity isolation of cell populations and (iv) fluorescence-activated cell sorting of cells labeled with a carbocyanine dye of acetylated low-density lipoprotein (DiI-Ac-LDL). Few criteria for selectively propagating pericytes (PC) are currently available.

Expression and subcellular distribution of filamin isotypes in endothelial cells and pericytes.

Two principal forms of the actin binding protein, filamin, are expressed in mammalian cells: nonmuscle and muscle isotypes (FLN-1 and FLN-2). A protein that copurifies with an alpha-naphthyl acetate hydrolyzing esterase from human omentum microvessel endothelial cells (EC) is isolated by nondenaturing electrophoresis, sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis and electroblotting. The purified protein is subjected to in situ trypsin cleavage, reversed-phase high performance liquid chromatography (HPLC) and automated Edman degradation.

Metabolites of the phospholipase D pathway regulate H2O2-induced filamin redistribution in endothelial cells.

Hypoxia/reoxygenation injury to cultured endothelial cells results in cytoskeletal rearrangement and second messenger activation related to increased monolayer junctional permeability. Cytoskeletal rearrangement by reactive oxygen species may be related to specific activation of the phospholipase D (PLD) pathway. Human umbilical vein endothelial cell monolayers are exposed to H2O2 (100 microM) or metabolites of the PLD pathway for 1-60 min.

Activation of endothelial cell kinin receptors leads to intracellular calcium increases and filamin translocation: regulation by protein kinase C.

Membrane-associated cytoskeletal proteins provide support for endothelial cell (EC) junctional cell adhesion molecules. Nonmuscle filamin is a dimeric actin cross-linking protein that interacts with F-actin and membrane glycoproteins. Both bradykinin and des-Arg9-bradykinin cause filamin redistribution from the plasma membrane to the cytosol of confluent EC.

Two-stage isolation procedure for obtaining homogenous populations of microvascular endothelial and mesothelial cells from human omentum.

The human omentum is a highly vascularized tissue often advocated as a source of human microvascular endothelial (HOME) cells. The omentum also contains mesothelial (MESO) cells and isolation protocols published to date do not describe a separation of the two cell populations. Using a two-stage collagenase digestion procedure, homogenous populations of HOME and MESO cells are obtained from the same omental tissue sample.

Human omental microvascular endothelial and mesothelial cells: characterization of two distinct mesodermally derived epithelial cells.

Human omental microvascular endothelial (HOME) and mesothelial (MESO) cells share many phenotypic properties, but can be characterized from one another based upon a comprehensive panel of endothelial and mesothelial markers. Traditional cell markers such as von-Willebrand factor, DiI-Ac-LDL, and Ulex europaeus I lectin are not sufficient to distinguish between HOME and MESO cells. Furthermore, immunoreactivity to a panel of endothelial cell-specific monoclonal antibodies, including representatives from the known clusters of differentiation (CD), indicate that some of these antigens are coexpressed in HOME and MESO cells.

H2O2-induced filamin redistribution in endothelial cells is modulated by the cyclic AMP-dependent protein kinase pathway.

Hypoxia/reoxygenation injury in vitro causes endothelial cell cytoskeletal rearrangement that is related to increased monolayer permeability. Nonmuscle filamin (ABP-280) promotes orthogonal branching of F-actin and links microfilaments to membrane glycoproteins. Human umbilical vein endothelial cell monolayers are exposed to H2O2 (100 microM) for 1-60 min, with or without modulators of cAMP-dependent second-messenger pathways, and evaluated for changes in filamin distribution, cAMP levels, and the formation of gaps at interendothelial junctions.

A novel anti-inflammatory peptide inhibits endothelial cell cytoskeletal rearrangement, nitric oxide synthase translocation, and paracellular permeability increases.

The endothelial cell (EC) membrane-cytoskeletal interface in part maintains plasma membrane integrity and promotes cell-cell apposition. Nonmuscle filamin (ABP-280), an actin crosslinking protein, promotes orthogonal branching of F-actin and is the major protein that links the peripheral actin network to the plasma membrane through its C-terminal glycoprotein binding site. In response to bradykinin, filamin translocates from the cell periphery to the cytosol within 1 min.

A luminescent europium complex for the sensitive detection of proteins and nucleic acids immobilized on membrane supports.

Certain metal complexes selectively interact with proteins immobilized on solid-phase membrane supports to form brightly colored products. Detecting the absorbance of colorimetric stains is limited by the molar extinction coefficient of the product, however. Development of light-emitting complexes should improve detection sensitivity, but fluorescent labels described to date modify free amino, carboxyl, or sulfhydryl groups often rendering proteins unsuitable for further analysis.

Antamanide Prevents Bradykinin-lnduced Filamin Translocation by Inhibiting Extracellular Calcium Influx.

Bradykinin-induced paracellular gap formation in cultured endothelial cells (ECs) is preceded by cytoskeletal rearrangement. Actin binding proteins, such as nonmuscle filamin, perform a pivotal role in modulating actin organization. In response to bradykinin treatment, EC filamin translocates from the cell periphery to the cytosol within 1 min and the dynamics of filamin translocation parallel intracellular Ca(2+) increases.

Filamin redistribution in an endothelial cell reoxygenation injury model.

Ischemia-reperfusion injury increases vascular permeability in part by generating reactive oxygen species that disassemble the endothelial cell actin dense peripheral band. This is followed by an increase in the number and diameter of intercellular gaps. Millimolar concentrations of reactive oxygen metabolites lead to nonspecific endothelial cell injury, but micromolar concentrations activate inflammatory second messenger cascades which produce distributional changes in endothelial cell cytoskeletal proteins.