Effect of Hydrothermal Aging on Damping Properties in Sisal Mat-Reinforced Polyester Composites.

Hydrothermal aging is a matter of considerable concern for natural fiber-reinforced polymers; it can alter dimensional stability and induce microcracks and macro strain on the composite structure. This study applied a sorption kinetic model and examined the effects of water on the damping factor of sisal mat-reinforced polyester composites. The experimental data were fitted well using a Boltzmann sigmoid function, suggesting a promising first step toward kinetic water sorption modeling. Additionally, a damping test was carried out using the impulse excitation technique, highlighting the composite material's dynamic response under varying water absorption conditions. The result showed that damping exhibited sensitivity to water absorption, increasing significantly during the first 24 h of immersion in water, then remained steady over time, inferring a critical time interval. An empirical model proved satisfactory with the correlation coefficient for sorption rates and damping of sisal mat polymeric composites.

Mast cell survival and mediator secretion in response to hypoxia.

Tissue hypoxia is a consequence of decreased oxygen levels in different inflammatory conditions, many associated with mast cell activation. However, the effect of hypoxia on mast cell functions is not well established. Here, we have investigated the effect of hypoxia per se on human mast cell survival, mediator secretion, and reactivity. Human cord blood derived mast cells were subjected to three different culturing conditions: culture and stimulation in normoxia (21% O(2)); culture and stimulation in hypoxia (1% O(2)); or 24 hour culture in hypoxia followed by stimulation in normoxia. Hypoxia, per se, did not induce mast cell degranulation, but we observed an increased secretion of IL-6, where autocrine produced IL-6 promoted mast cell survival. Hypoxia did not have any effect on A23187 induced degranulation or secretion of cytokines. In contrast, cytokine secretion after LPS or CD30 treatment was attenuated, but not inhibited, in hypoxia compared to normoxia. Our data suggests that mast cell survival, degranulation and cytokine release are sustained under hypoxia. This may be of importance for host defence where mast cells in a hypoxic tissue can react to intruders, but also in chronic inflammations where mast cell reactivity is not inhibited by the inflammatory associated hypoxia.

CD153 in rheumatoid arthritis: detection of a soluble form in serum and synovial fluid, and expression by mast cells in the rheumatic synovium.

OBJECTIVE: A CD30-CD153 mast cell axis has been described in skin inflammations and Hodgkin's lymphoma. We investigated if a soluble form of CD153 is present in the serum and synovial fluid (SF) of patients with rheumatoid arthritis (RA), and determined whether mast cells express CD153 in the synovium of these patients. METHODS: Soluble forms of CD30 and CD153 were quantified in serum and SF of patients with RA by ELISA. Consecutive sections of synovial biopsies from 12 patients were stained against tryptase (mast-cell marker), CD30, and CD153. RESULTS: Elevated concentrations of the soluble form of CD153 were found in serum from 14/15 RA patients. In the SF, 11/20 patients had detectable levels of soluble CD153. CD30 and CD153 were expressed in all biopsies that were studied. Mast cells were present in all the synovial biopsies, and expressed CD153 in one-third of the cases. CONCLUSION: We observed that CD153 was expressed in the synovium of patients with RA and we were able to correlate the serum levels of soluble CD153 with SF levels in the same patients. Because CD30 can activate mast cells to release chemokines without degranulation, our finding that mast cells express CD153 in RA synovium raises the possibility that a CD30-CD153 axis may contribute to the activation of synovial mast cells in the absence of degranulation.

Expression of mast cell tryptases in Hodgkin and Reed-Sternberg (HRS) cells.

Tryptase is the most abundant protease in human mast cells, and is often used as a marker for the enumeration of mast cells in tissue. Here we report that tumour cells from Hodgkin lymphoma, the so called Hodgkin and Reed-Sternberg cells, can express tryptase. Hodgkin lymphoma cell lines expressed mRNA for both alpha- and beta-tryptase and also produced the protein, although at much lower concentrations than mast cells. However, the frequency of tryptase positive HRS-cells in situ was very low. This report demonstrates that tumour cells of lymphoid origin can express tryptase in vitro and in situ.

BDNF regulates the expression and traffic of NMDA receptors in cultured hippocampal neurons.

The neurotrophin BDNF regulates the activity-dependent modifications of synaptic strength in the CNS. Physiological and biochemical evidences implicate the NMDA glutamate receptor as one of the targets for BDNF modulation. In the present study, we investigated the effect of BDNF on the expression and plasma membrane abundance of NMDA receptor subunits in cultured hippocampal neurons. Acute stimulation of hippocampal neurons with BDNF differentially upregulated the protein levels of the NR1, NR2A and NR2B NMDA receptor subunits, by a mechanism sensitive to transcription and translation inhibitors. Accordingly, BDNF also increased the mRNA levels for NR1, NR2A and NR2B subunits. The neurotrophin NT3 also upregulated the protein levels of NR2A and NR2B subunits, but was without effect on the NR1 subunit. The amount of NR1, NR2A and NR2B proteins associated with the plasma membrane of hippocampal neurons was differentially increased by BDNF stimulation for 30 min or 24 h. The rapid upregulation of plasma membrane-associated NMDA receptor subunits was correlated with an increase in NMDA receptor activity. The results indicate that BDNF increases the abundance of NMDA receptors and their delivery to the plasma membrane, thereby upregulating receptor activity in cultured hippocampal neurons.

Mast cell CD30 ligand is upregulated in cutaneous inflammation and mediates degranulation-independent chemokine secretion.

Mast cells are involved in many disorders where the triggering mechanism that leads to degranulation and/or cytokine secretion has not been defined. Several chronic inflammatory diseases are associated with increased mast cell numbers and upregulation of the TNF receptor family member CD30, but the role of elevated CD30 expression is poorly understood. Here we report what we believe to be a novel way to activate mast cells with CD30 that leads to degranulation-independent secretion of chemokines. CD30 induced a de novo synthesis and secretion of the chemokines IL-8, macrophage inflammatory protein-1alpha (MIP-1alpha), and MIP-1beta, a process involving the MAPK/ERK pathway. Mast cells were found to be the predominant CD30 ligand-positive (CD30L-positive) cell in the chronic inflammatory skin diseases psoriasis and atopic dermatitis, and both CD30 and CD30L expression were upregulated in lesional skin in these conditions. Furthermore, the number of IL-8-positive mast cells was elevated both in psoriatic and atopic dermatitis lesional skin as well as in ex vivo CD30-treated healthy skin organ cultures. In summary, characterization of CD30 activation of mast cells has uncovered an IgE-independent pathway that is of importance in understanding the entirety of the role of mast cells in diseases associated with mast cells and CD30 expression. These diseases include Hodgkin lymphoma, atopic dermatitis, and psoriasis.

Silencing of EphA3 through a cis interaction with ephrinA5.

EphAs and ephrinAs are expressed in multiple areas of the developing brain in overlapping countergradients, notably in the retina and tectum. Here they are involved in targeting retinal axons to their correct topographic position in the tectum. We have used truncated versions of EphA3, single-amino acid point mutants of ephrinA5 and fluorescence resonance energy transfer technology to uncover a cis interaction between EphA3 and ephrinA5 that is independent of the established ligand-binding domain of EphA3. This cis interaction abolishes the induction of tyrosine phosphorylation of EphA3 and results in a loss of sensitivity of retinal axons to ephrinAs in trans. Our data suggest that formation of this complex transforms the uniform expression of EphAs in the nasal part of the retina into a gradient of functional EphAs and has a key role in controlling retinotectal mapping.