Staphylococcus aureus-Fibronectin Interactions with and without Fibronectin-Binding Proteins and Their Role in Adhesion and Desorption

Adhesion and residence-time-dependent desorption of two Staphylococcus aureus strains with and without fibronectin (Fn) binding proteins (FnBPs) on Fn-coated glass were compared under flow conditions. To obtain a better understanding of the role of Fn-FnBP binding, the adsorption enthalpies of Fn with staphylococcal cell surfaces were determined using isothermal titration calorimetry (ITC). Interaction forces between staphylococci and Fn coatings were measured using atomic force microscopy (AFM). The strain with FnBPs adhered faster and initially stronger to an Fn coating than the strain without FnBPs, and its Fn adsorption enthalpies were higher. The initial desorption was high for both strains but decreased substantially within 2 s. These time scales of staphylococcal bond ageing were confirmed by AFM adhesion force measurement. After exposure of either Fn coating or staphylococcal cell surfaces to bovine serum albumin (BSA), the adhesion of both strains to Fn coatings was reduced, suggesting that BSA suppresses not only nonspecific but also specific Fn-FnBP interactions. Adhesion forces and adsorption enthalpies were only slightly affected by BSA adsorption. This implies that under the mild contact conditions of convective diffusion in a flow chamber, adsorbed BSA prevents specific interactions but does allow forced Fn-FnBP binding during AFM or stirring in ITC. The bond strength energies calculated from retraction force-distance curves from AFM were orders of magnitude higher than those calculated from desorption data, confirming that a penetrating Fn-coated AFM tip probes multiple adhesins in the outermost cell surface that remain hidden during mild landing of an organism on an Fn-coated substratum, like that during convective diffusional flow

Rotor-position detection in permanent-magnet wheel motor to ensure smooth startup from standstill

In this paper, an innovative rotor-position-detection method for a permanent-magnet wheel motor (PMWM) that operates from standstill to low speed is presented. The neutral voltage, which is sensed through phaseshifted pulse width modulation, overcomes the limitations of the conventional back electromotive force (EMF)-based position-detection method, which is more suitable for high-speed operation. In addition, a technique that ensures a transition between the two position-detection methods is presented to cover the full speed range. Computer simulations are employed to design and assess the neutral-voltage-based and EMF-based position-detection methods. The results of the position detection and angle error are presented starting from standstill to low speed. A step current (iq) corresponding to motor torque demand is applied for the starting process in the two position-detection methods. The experimental studies of the new position-detection method are conducted. The method is successfully applied to drive a 60-kW PMWM that operates from standstill to high speed. This demonstrates the effectiveness and performance of the presented method

Attenuating Diabetic Vascular and Neuronal Defects by Targeting P2rx7.

Retinal vascular and neuronal degeneration are established pathological features of diabetic retinopathy. Data suggest that defects in the neuroglial network precede the clinically recognisable vascular lesions in the retina. Therefore, new treatments that target early-onset neurodegeneration would be expected to have great value in preventing the early stages of diabetic retinopathy. Here, we show that the nucleoside reverse transcriptase inhibitor lamivudine (3TC), a newly discovered P2rx7 inhibitor, can attenuate progression of both neuronal and vascular pathology in diabetic retinopathy. We found that the expression of P2rx7 was increased in the murine retina as early as one month following diabetes induction. Compared to non-diabetic controls, diabetic mice treated with 3TC were protected against the formation of acellular capillaries in the retina. This occurred concomitantly with a maintenance in neuroglial function, as shown by improved a- and b-wave amplitude, as well as oscillatory potentials. An improvement in the number of GABAergic amacrine cells and the synaptophysin-positive area was also observed in the inner retina of 3TC-treated diabetic mice. Our data suggest that 3TC has therapeutic potential since it can target both neuronal and vascular defects caused by diabetes

IL-33 deficiency causes persistent inflammation and severe neurodegeneration in retinal detachment.

BACKGROUND: Interleukin-33 (IL-33) belongs to the IL-1 cytokine family and resides in the nuclei of various cell types. In the neural retina, IL-33 is predominately expressed in Müller cells although its role in health and disease is ill-defined. Müller cell gliosis is a critical response during the acute phase of retinal detachment (RD), and in this study, we investigated if IL-33 was modulatory in the inflammatory and neurodegenerative pathology which is characteristic of this important clinical condition. METHODS: RD was induced by subretinal injection of sodium hyaluronate into C57BL/6 J (WT) and IL-33-/- mice and confirmed by fundus imaging and optical coherence tomography (OCT). The expression of inflammatory cytokines, complement components and growth factors was examined by RT-PCR. Retinal neurodegeneration, Müller cell activation and immune cell infiltration were assessed using immunohistochemistry. The expression of inflammatory cytokines in primary Müller cells and bone marrow-derived macrophages (BM-DMs) was assessed by RT-PCR and Cytometric Bead Array. RESULTS: RD persisted for at least 28 days after the injection of sodium hyaluronate, accompanied by significant cone photoreceptor degeneration. The mRNA levels of CCL2, C1ra, C1s, IL-18, IL-1β, TNFα, IL-33 and glial fibrillary acidic protein (GFAP) were significantly increased at day 1 post-RD, reduced gradually and, with the exception of GFAP and C1ra, returned to the basal levels by day 28 in WT mice. In IL-33-/- mice, RD induced an exacerbated inflammatory response with significantly higher levels of CCL2, IL-1β and GFAP when compared to WT. Sustained GFAP activation and immune cell infiltration was detected at day 28 post-RD in IL-33-/- mice. Electroretinography revealed a lower A-wave amplitude at day 28 post-RD in IL-33-/- mice compared to that in WT RD mice. IL-33-/- mice subjected to RD also had significantly more severe cone photoreceptor degeneration compared to WT counterparts. Surprisingly, Müller cells from IL-33-/- mice expressed significantly lower levels of CCL2 and IL-6 compared with those from WT mice, particularly under hypoxic conditions, whereas IL-33-/- bone marrow-derived macrophages expressed higher levels of inducible nitric oxide synthase, TNFα, IL-1β and CCL2 after LPS + IFNγ stimulation compared to WT macrophages. CONCLUSION: IL-33 deficiency enhanced retinal degeneration and gliosis following RD which was related to sustained subretinal inflammation from infiltrating macrophages. IL-33 may provide a previously unrecognised protective response by negatively regulating macrophage activation following retinal detachment

Strongly coupled matter near phase transition

In the Hartree approximation of Cornwall-Jackiw-Tomboulis (CJT) formalism of the real scalar field theory, we show that for the strongly coupled scalar system near phase transition, the shear viscosity over entropy density is small, however, the bulk viscosity over entropy density is large. The large bulk viscosity is related to the highly nonconformal equation of state. It is found that the square of the sound velocity near phase transition is much smaller than the conformal value 1/3, and the trace anomaly at phase transition deviates far away from 0. These results agree well with the lattice results of the complex QCD system near phase transition.Comment: 6 pages, 2 figures, 1 table, contributed to the International Conference on Strangeness in Quark Matter 2008, Beijing, China, 6-10 October 200

Multi-stage learning for segmentation of aortic dissections using a prior aortic anatomy simplification

Aortic dissection (AD) is a life-threatening cardiovascular disease with a high mortality rate. The accurate and generalized 3-D reconstruction of AD from CT-angiography can effectively assist clinical procedures and surgery plans, however, is clinically unavaliable due to the lacking of efficient tools. In this study, we presented a novel multi-stage segmentation framework for type B AD to extract true lumen (TL), false lumen (FL) and all branches (BR) as different classes. Two cascaded neural networks were used to segment the aortic trunk and branches and to separate the dual lumen, respectively. An aortic straightening method was designed based on the prior vascular anatomy of AD, simplifying the curved aortic shape before the second network. The straightening-based method achieved the mean Dice scores of 0.96, 0.95 and 0.89 for TL, FL, and BR on a multi-center dataset involving 120 patients, outperforming the end-to-end multi-class methods and the multi-stage methods without straightening on the dual-lumen segmentation, even using different network architectures. Both the global volumetric features of the aorta and the local characteristics of the primary tear could be better identified and quantified based on the straightening. Comparing to previous deep learning methods dealing with AD segmentations, the proposed framework presented advantages in segmentation accuracy