A novel group of Moraxella catarrhalis UspA proteins mediates cellular adhesion via CEACAMs and vitronectin.

Moraxella catarrhalis (Mx) is a common cause of otitis media and exacerbation of chronic obstructive pulmonary disease, an increasing worldwide problem. Surface proteins UspA1 and UspA2 of Mx bind to a number of human receptors and may function in pathogenesis. Genetic recombination events in the pathogen can generate hybrid proteins termed UspA2H.

Chondrocyte death by apoptosis is associated with the initiation and severity of articular cartilage degradation.

Aim: To investigate the role of chondrocyte apoptosis in the initiation and severity of articular cartilage (AC) damage.

Methods: Articular cartilage from equine metacarpophalangeal (MCP) (n = 13) and metatarsophalangeal (MTP) (n = 16) joints was used and each graded macroscopically for cartilage degradation (macroscopic osteoarthritis [OA] grade). Cartilage was sampled from six regions on the articular surface of both joint types and graded using a 'modified' Mankin scoring system.

Variations in chondrocyte apoptosis may explain the increased prevalence of osteoarthritis in some joints.

Objectives: To investigate whether there are any variations in chondrocyte susceptibility to an apoptotic stimulus between cells of articular cartilage (AC) from equine joints that differ in prevalence of osteoarthritis (OA).

Methods: Cartilage from macroscopically normal equine metacarpophalangeal (MCP), proximal interphalangeal (PIP) and distal interphalangeal (DIP) joints was used. Prior to culture, chondrocyte viability was assessed using the fluorescein diacetate (FDA) and propidium iodide paravital staining method.

A 5-yr longitudinal study of type IIA collagen synthesis and total type II collagen degradation in patients with knee osteoarthritis--association with disease progression.

Objectives: The 5-yr longitudinal study tested the hypothesis that serum and urinary markers of type II collagen metabolism would be associated with radiological progression of disease in patients with mild-to-moderate knee osteoarthritis (OA).

Methods: Synthesis of type IIA collagen and degradation of total type II collagen were assessed in 135 patients with mild-to-moderate knee OA over 5 yrs using serum concentration of the N-propeptide of collagen type IIA (PIIANP) and urinary excretion of crosslinked C-telopeptide (CTX-II), respectively. The markers were measured at baseline, 2, 3 and 5 yrs' follow-up corresponding to X-ray time points.

Chondrocyte death by apoptosis is associated with cartilage matrix degradation.

Objectives: To investigate the frequency of chondrocyte apoptosis in equine articular cartilage (AC) specimens and to examine the relationship between the process of cell death and the degree of cartilage degradation using a direct quantification of numbers of apoptotic cells and expression of active caspase-3.

Methods: AC from equine metacarpophalangeal (MCP), proximal interphalangeal (PIP) and distal interphalangeal (DIP) joints was used and each joint was graded macroscopically for cartilage degradation (macroscopic osteoarthritis (OA) score). Cartilage sections were graded using a 'modified' Mankin scoring system.

VEGF165b, an inhibitory vascular endothelial growth factor splice variant: mechanism of action, in vivo effect on angiogenesis and endogenous protein expression.

Growth of new blood vessels (angiogenesis), required for all tumor growth, is stimulated by the expression of vascular endothelial growth factor (VEGF). VEGF is up-regulated in all known solid tumors but also in atherosclerosis, diabetic retinopathy, arthritis, and many other conditions. Conventional VEGF isoforms have been universally described as proangiogenic cytokines.

An adenovirus-mediated gene-transfer model of angiogenesis in rat mesentery.

Objective: To develop an adenovirus-mediated angiogenesis model, dependent on VEGF, in a system amenable to functional characterization.

Methods: Adenovirus (AdV) expressing VEGF (Ad-VEGF) or GFP (Ad-EGFP) (1-3.3 x 10(8) TCID50/mL), and Monastral blue were injected into the fat pad on either side of a mesenteric connective tissue panel of halothane-anesthetized male Wistar rats after intravital microscopic imaging.

ZM323881, a novel inhibitor of vascular endothelial growth factor-receptor-2 tyrosine kinase activity.

Objective: Vascular endothelial growth factor (VEGF) increases vascular permeability and angiogenesis in many pathological conditions including cancer, arthritis, and diabetes. VEGF activates VEGF-Receptor 1(VEGF-R1) and VEGF-Receptor 2 (VEGF-R2), which autophosphorylate to initiate a signaling cascade resulting in angiogenesis and increased microvascular permeability. Here we describe a novel VEGF-R2 selective inhibitor, ZM323881 (5-[[7-(benzyloxy) quinazolin-4-yl]amino]-4-fluoro-2-methylphenol), that is a potent and selective inhibitor of VEGF-R2 tyrosine kinase in vitro (IC(50) < 2 nM), compared with other receptor tyrosine kinases, including VEGF-R1 (IC(50) > 50 microM).

Differential effects of vascular endothelial growth factor-C and placental growth factor-1 on the hydraulic conductivity of frog mesenteric capillaries.

Vascular endothelial growth factors (VEGFs) are known to increase vascular permeability. VEGF-A acts on two receptor tyrosine kinases, VEGF receptor-1 (VEGF-R1 or flt-1) and VEGF receptor-2 (VEGF-R2, flk-1 or KDR). VEGF-C acts only on VEGF-R2 on vascular endothelial cells, whereas placental growth factor-1 (PlGF-1) acts only on VEGF-R1.

Apoptotic and proliferative activity in the neoplastic progression of Barrett's oesophagus: a comparative study.

The balance between proliferation and apoptosis within a tissue is important in controlling its overall growth. When either or both are altered, uncontrolled cell proliferation can contribute to cancer. The aim of this study was to investigate apoptosis and proliferation in the progression from Barrett's oesophagus to adenocarcinoma.