P waves Characterization by WaveletTransform

PwavesinElectrocardiography(ECG)containtheimportantinformationofelectricalactivitiesfromatrial-sinusnode,rightandleftatrium1.2BecauseofthelowamplitudeofthesesignalsandthenoisesinterferencethecharacteristicsofthePwavehasnotbeenwellstudied.Wedevelopedasystemtode-noiseandamplifythep-wavesignals,andtemporalcharacteristicsofPwaveswereanalyzedbyusingwavelettransform.1.MethodElectrocardiograghyfrom60youngmenwithnormalbloodpressureand12-leadECGresultswererecordedandthende-noisedbysoftthresholdingt…     

Hepatitis-like syndrome induced by nimesulide?

The authors describe a case report of a 17 years old woman, complaining of weakness and malaise, associated with a significant increase of serum transaminases, that occurred twice in a month soon after the administration of Nimesulide per o.s.     

Body-barrier surveillance by epidermal γδ TCRs

The surveillance of body barriers relies on resident T cells whose repertoires are biased toward particular γδ T cell antigen receptors (TCRs) according to location. These γδ TCRs can recognize ligands that emerge after stress. Through the use of intravital dynamics-immunosignal correlative microscopy, we found that γ-chain variable region 5 (V(γ)5) TCRs expressed by epidermal T cells were constitutively clustered and functionally activated in vivo at steady state, forming true immunological synapses that polarized and anchored T cell projections at squamous keratinocyte tight junctions. This synaptogenesis depended on TCR variable domains, the kinase Lck and the integrin α(E)β(7) but not the γδ lineage or the receptor NKG2D. In response to tissue stress, TCR-proximal signals did not increase substantially but underwent stress mode-dependent relocalization toward the basal epidermis and Langerhans cells. Thus, the γδ TCR orchestrates barrier surveillance proactively, presumably by recognizing tissue ligands expressed in the steady state.     

Patterning proteins on surfaces by micro-channels

Microfabrication,the generation of small structures is essential for much of themodern science and technology.Traditional technology of lithography is expensiveand limited to generate micropattern on surfaces of materials.Recently,anotherkind of technology of so- called soft- lithography is developed.In our current work,we firstly observe the interaction of biotinylated BSA and avidin,and then createspatially specific micropattern of biotinylated BSA on surfaces.The ultimate goal isto selec…     

Activation of an apical Cl– conductance by extracellular ATP in Necturus gallbladder is mediated by cAMP and not by [Ca2+]i

Necturus gallbladder epithelium (NGE) expresses a CFTR-like apical Cl- conductance that can be activated by cAMP. Here, we show that extracellular ATP (100 microM), which is known to elevate intracellular Ca2+ and to hyperpolarize cells by stimulating apical and basolateral K+ conductances, also stimulates an apical Cl- conductance (Ga,Cl), however with a much slower time course. The selectivity sequence of Ga,Cl was SCN- > I- > NO3- > Br- > Cl- > isethionate (ISE-), but SCN- and I- partially blocked it, which is analogous to observations of CFTR Cl- channels. To disclose a possible role for intracellular Ca2+, gallbladders were incubated with the Ca2+ chelator BAPTA/AM or bathed in solutions containing only submicromolar Ca2+ concentrations. BAPTA partially inhibited the Ca(2+)-mediated hyperpolarization, but did not reduce the ATP-dependent activation of Ga,Cl and the latter was also seen in low extracellular Ca2+. On the other hand, the cAMP-antagonist Rp-8-Br-cAMPS strongly inhibited the stimulation of Ga,Cl by ATP (as well as by forskolin), but left the ATP-induced hyperpolarization unchanged. Preincubation with a low concentration of forskolin markedly enhanced the stimulatory effect of ATP, and this effect was not modified by the selective inhibition of protein kinase C. These data suggest the involvement of different signal transduction pathways in the ATP-dependent activation of K+ and Cl- conductances in NGE. The stimulation of the Ga,Cl appears to be mediated by cAMP but not by elevation of intracellular Ca2+.     

Enhanced Phosphorylation of MAPKs by NE Promotes TNF-α Production by Macrophage Through α Adrenergic Receptor

The aim of this study was to investigate whether norepinephrine (NE) could regulate macrophage production of tumor necrosis factor alpha (TNF-α) by influencing the phosphorylation of mitogen-activated protein kinases (MAPKs). Primary macrophages from male BALB/c mice were applied to explore the mechanism by which NE influences the the secretion of TNF-α when macrophages were activated by lipopolysaccharides (LPS). We found that NE could increase crophage production of TNF-α when macrophages were activated by LPS, and this effect could be inhibited by α adrenergic antagonist phentolamine. Also, NE could increase the phosphorylation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinases (ERK), and p38, through α receptor. Furthermore, JNK inhibitor SP600125, ERK inhibitor U0126, and p38 inhibitor SB203580 could all partially counteract NE’s effect on the phosphorylation of MAPKs, as well as TNF-α production by macrophages. This study revealed that as macrophages were activated by LPS, NE promoted the secretion of inflammatory factors by increasing the phosphorylation of MAPKs through an α receptor-dependent pathway. Our results provide the evidence of a relationship between stress and diseases, as well as the mechanism by which stress induces or affects the inflammation-related diseases.     

VEGF Production by Osteoarthritic Chondrocytes Cultured in Micromass and Stimulated by IL-17 and TNF-α

We compared the secretion of vascular endothelial growth factor (VEGF) by chondrocytes isolated from cartilage of patients with osteoarthritis (OA) and maintained in monolayer or in three-dimensional culture. Chondrocytes, immediately after isolation, or after one passage in monolayer culture (subculture), were seeded in monolayer or pelleted in micromasses. Cells cultured differently were immunoassayed for the secretion of VEGF in basal conditions or after stimulation with IL-17, TNF-α or B IL-17+TNF-α. Chondrocytes cultured in micromasses secreted lower levels of VEGF in comparison with those in monolayer culture. In micromass cultures TNF-α was more stimulating than IL-17 and their combined effect was additional. On the basis of alkaline phosphatase/cathespin B activities, primary cultures in micromass, characterized by low VEGF secretion, represented the best condition for maximal cell differentiation. Our results suggest that the culture of chondrocytes in micromasses represents a good condition to study the physiology of these cells to a maximum degree when micromasses are obtained with freshly isolated chondrocytes.     

Neutrophil Migration Induced by IL-1β Depends upon LTB4 Released by Macrophages and upon TNF-α and IL-1β Released by Mast Cells

In the present study, we investigate whether mast cells and macrophages are involved in the control of IL-1β-induced neutrophil migration, as well as the participation of chemotactic mediators. IL-1β induced a dose-dependent neutrophil migration to the peritoneal cavity of rats which depends on LTB₄, PAF and cytokines, since the animal treatment with inhibitors of these mediators (MK 886, PCA 4248 and dexamethasone respectively) inhibited IL-1β-induced neutrophil migration. The neutrophil migration induced by IL-1β is dependent on mast cells and macrophages, since depletion of mast cells reduced the process whereas the increase of macrophage population enhanced the migration. Moreover, mast cells or macrophages stimulated with IL-1β released a neutrophil chemotactic factor, which mimicked the neutrophil migration induced by IL-1β. The chemotactic activity of the supernatant of IL-1β-stimulated macrophages is due to the presence of LTB₄, since MK 886 inhibited its release. Moreover, the chemotactic activity of IL-1β-stimulated mast cells supernatant is due to the presence of IL-1β and TNF-α, since antibodies against these cytokines inhibited its activity. Furthermore, significant amounts of these cytokines were detected in the supernatant. In conclusion, our results suggest that neutrophil migration induced by IL-1β depends upon LTB₄ released by macrophages and upon IL-1β and TNFα released by mast cells.     

Quantifying Rosette Formation Mediated by Receptor-ligand Interactions

1 IntroductionRosetting is a simple assay for specific cell-cell adhesion, in which receptor- (or ligand-) coated RBCs form the rosettes with ligand- (or receptor-) expressed nucleated cells~([1]). Although routinely used by immunologists to examine the functionality of the interacting receptors and ligands, however, it has not been regarded as a quantitative method, as the measured rosette fraction has not been quantitatively related to the underlying molecular properties.Recently, we have s…     

Is infection by Dermatophilus congolensis underdiagnosed?

Dermatophilus congolensis, which affects animal species, is an uncommon human infection. Few cases, mainly in tropical areas, have been reported. We describe the first human infection in Spain in a traveler returning from Central America. Diagnosis of human infection may be underestimated in people in contact with animals.