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We derived analytical formula for the cross-spectral density of a radially polarized partially coherent twist (RPPCT) beam propagating in a uniaxial crystal orthogonal to the optical axis with the help of the extended Huygens-Fresnel integral formula and unified theory of coherence and polarization. Furthermore, we explore the evolution properties of a RPPCT beam propagating in a uniaxial crystal. It is found that the RPPCT beam becomes an anisotropic RPPCT beam and the beam spot is rotating with beam propagation in uniaxial crystal. Its evolution properties change with twist factor and the ratio of extraordinary index to ordinary refractive index. The twist factor affects their rotation orientation angles, and the ratio of extraordinary index to ordinary refractive index has an effect on their twisted levels. Graphical abstract: [ABSTRACT FROM AUTHOR]

Lysophosphatidic acid (LPA) is a bioactive phospholipid that activates at least five known G-protein-coupled receptors (GPCRs): LPA1-LPA5. The nervous system is a major locus for LPA1 expression. LPA has been shown to regulate neuronal proliferation, migration, and differentiation during central nervous system development as well as neuronal survival. Furthermore, deficient LPA signaling has been implicated in several neurological disorders including neuropathic pain and schizophrenia. Parkinson's disease (PD) is a neurodegenerative movement disorder that results from the loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNc). The specific molecular pathways that lead to DA neuron degeneration, however, are poorly understood. The influence of LPA in the differentiation of mesenchymal stem cells (MSCs) into DA neurons in vitro and LPA1 expression in a 6-hydroxydopamine (6-OHDA) lesion model of PD in vivo were examined in the present study. LPA induced neuronal differentiation in 80.2 % of the MSC population. These MSCs developed characteristic neuronal morphology and expressed the neuronal marker, neuron-specific enolase (NSE), while expression of the glial marker, glial fibrillary acidic protein (GFAP), was absent. Moreover, 27.6 % of differentiated MSCs were positive for tyrosine hydroxylase (TH), a marker for DA neurons. In the 6-OHDA PD rat model, LPA1 expression in the substantia nigra was significantly reduced compared to control. These results suggest LPA signaling via activation of LPA1 may be necessary for DA neuron development and survival. Furthermore, reduced LPA/LPA1 signaling may be involved in DA neuron degeneration thus contributing to the pathogenesis of PD. [ABSTRACT FROM AUTHOR]

The pigmentation of mammalian skin and hair develops through the interaction of two basic cell types - pigment donors and recipients. The pigment donors are melanocytes, which produce and distribute melanin through specialized structures. The pigment recipients are epithelial cells, which acquire melanin and put it to use, collectively yielding the pigmentation visible to the eye. This review will focus on the pigment recipients, the historically less understood cell type. These end-users of pigment are now known to exert a specialized control over the patterning of pigmentation, as they identify themselves as melanocyte targets, recruit pigment donors, and stimulate the transfer of melanin. As such, this review will discuss the evidence that the skin is like a coloring book: the pigment recipients create a 'picture,' a blueprint for pigmentation, which is colorless initially but outlines where pigment should be placed. Melanocytes then melanize the recipients and 'color in' the picture. [ABSTRACT FROM AUTHOR]

Objective: To investigate the biochemical changes in striatum after rat bone marrow mesenchymal stem cells (MSCs) were transplanted into hemiparkinsonian rats and to further confirm the therapeutic effects of rat MSCs for Parkinson's disease (PD). Methods: 5-bromo-2-deoxyuridine (BrdU)-labeled MSCs were transplanted into the corpus striatum of the 6-hydroxydopamine (6-OHDA)-injected side of six PD model rats. Before and 8 weeks after MSC transplantation, ethological changes in PD rats were assessed. The expression of tyrosine hydroxylase (TH) in substantia nigra (SN) and striatum were measured using immunohistochemical methods. The differentiation of MSCs was detected by double immunofluorescence techniques. The concentrations of neural metabolites of N-acetylaspartate (NAA), choline (Cho) and creatine (Cr) were measured by 1H-magnetic resonance spectroscopy (MRS). Relative concentrations of NAA/Cr and Cho/Cr were calculated. Results: The behavior of PD rats in rotarod tests improved, and there were statistical differences in TH-positive cells in SN and TH-positive terminals in striatum after the transplantation of BrdU-labeled MSCs. Transplanted MSCs differentiated into MAP-2-positive neurons. Especially compared with pre-MSC transplantation, the neural metabolite NAA/Cr ratio of the 6-OHDA-injected side of the striatum increased ( P < 0.05) and the Cho/Cr ratio decreased ( P < 0.05). Conclusion: MSCs transplantation apparently improves neuronal function in the striatum of PD rats. [ABSTRACT FROM AUTHOR]

On the basis of the extended Huygens–Fresnel integral principle and unified theory of coherence and polarization of light, we studied the effects of oceanic turbulence on polarization properties of a partially coherent radially polarized doughnut (PCRPD) beam. The ocean-induced fluctuations in the refractive index are assumed be driven by temperature and salinity fluctuations. Numerical examples of changes in polarization properties, such as the degree of polarization, the degree of ellipticity, and the orientation angle in the oceanic turbulence for the PCRPD beam, are given. Our analysis demonstrates how polarization of the PCRPD beam is affected by statistical properties of the source and by several parameters of oceanic turbulence. We find that the propagation of the PCRPD beam is different from that of stochastic beams in oceanic turbulence. The degree of polarization for the PCRPD beam approaches a certain steady value, and the elliptical polarized state of the fully polarized portion of the beam will become fully linear in the far field. [ABSTRACT FROM PUBLISHER]

Microcystin-LR (MCLR) is one of the most common and most toxic members of the microcystins, which cause serious environmental disasters worldwide. Although the major toxicity of MCLR has been ascribed to its potent ability to inhibit protein phosphatase 1 and protein phosphatase 2A (PP2A), recent studies have suggested that MCLR may also perturb other important cellular processes, such as generation of ceramide. Ceramide is an essential second messenger in cells and regulates various cellular mechanisms, including PP2A activation and cytoskeleton destabilization. However, whether and how ceramide may mediate MCLR-induced cellular effects is unclear. We have previously reported that low concentrations of MCLR upregulate, rather than inhibit, PP2A activity in human embryonic kidney 293 (HEK293) cells. In this study, we provide evidence that MCLR induces ceramide generation in HEK293 cells and in mouse kidney. Furthermore, ceramide may mediate the MCLR-induced upregulation of PP2A activity and protein level of PP2A regulatory subunits in HEK293 cells. MCLR intoxication also causes the PP2A/B55α subunit to localize to the Golgi apparatus, and this process may also be mediated by ceramide. Importantly, ceramide may mediate cytoskeleton destabilization, cell detachment, and apoptosis induced by MCLR in HEK293 cells, whereas a ceramide synthase inhibitor, desipramine, protects cells from these changes. Our results suggest that ceramide may mediate MCLR-induced PP2A regulation and cytoskeleton destabilization. [ABSTRACT FROM PUBLISHER]

Patient-specific models are widely used in hemodynamic simulations. The flow in the boundary layer changes so strongly that fine meshes in the boundary layer are required in numerical simulations, especially for the calculation of wall shear stress and its gradient. To precisely analyze hemodynamics, it is necessary to investigate the approaches to the reconstruction of a numerical simulation-oriented patient-specific model for aortic arch aneurysm that can perform particular meshing in the boundary layer. Based on a surface model of aortic arch aneurysm in STL format, reverse engineering concept was applied to reconstruct a solid model using CAD software Geomagic and Pro/E, and a simplified model of stent for the intervention of aortic arch aneurysm was also created. After these models were imported to ANSYS, a block modeling approach was employed to divide the whole model into several domain blocks to adopt different meshing strategies. Particular meshing was performed especially in the boundary layer and around the stents. The finite element model particularly suitable for numerical simulation of hemodynamics was obtained. Hemodynamic simulation was performed, using the constructed finite element model to verify its applicability. The results indicate that reverse engineering concept and the proposed block modeling approach can be used to divide the solid model of aortic arch aneurysm into multiple volumes, which can be meshed according to particular requirements in each volume; the finite element model of stented aortic arch aneurysm can be employed to simulate hemodynamics. The approaches of modeling were applicable not only for aortic arch aneurysm, but also for similar model reconstruction as a reference in hemodynamic simulation investigations. [ABSTRACT FROM AUTHOR]

The conventional dynamic programming-based track-before-detect (DP-TBD) methods are usually intractable in multi-target scenarios. The adjacent targets may interfere with each other, and the computational complexity is increased with the number of targets. In this paper, a DP-TBD method using parallel computing (PC-DP-TBD) is proposed to solve the above problems. The search region of the proposed PC-DP-TBD is divided into several parts according to the possible target movement direction. The energy integration is carried out independently and parallel in each part. This contributes to reducing the computational complexity in each part, since the divided search region is smaller than the whole one. In addition, the target energy can only be integrated adequately in the part in which the search direction matches the target movement. This is beneficial to improve the ability to detect the targets with various movement directions in different parts with different search directions. The solution to the problem of the adjacent targets interfering with each other is discussed. The procedure of the parallel computing in the proposed PC-DP-TBD is presented in detail. Simulations are conducted to verify the superiority of the proposed PC-DP-TBD in terms of detection probability and computational complexity. [ABSTRACT FROM AUTHOR]

The article presents abstracts on pigment cell research presented at the 16th Meeting of the European Society for Pigment Cell Research, which include the development and functions of retinal pigment epithelium cells, the regulation of epidermal stem cells in mammalian epidermis, and the biological modeling of melanocyte development.

TNFR1 and TNFR2 have received prominent attention because of their dominance in the pathogenesis of inflammation and autoimmunity. TNFR1 has been extensively studied and primarily mediates inflammation. TNFR2 remains far less studied, although emerging evidence demonstrates that TNFR2 plays an antiinflammatory and immunoregulatory role in various conditions and diseases. Herein, we report that TNFR2 regulates macrophage polarization, a highly dynamic process controlled by largely unidentified intracellular regulators. Using biochemical copurification and mass spectrometry approaches, we isolated the signaling molecule 14-3-3[epsilon] as a component of TNFR2 complexes in response to progranulin stimulation in macrophages. In addition, 14-3-3[epsilon] was essential for TNFR2 signaling-mediated regulation of macrophage polarization and switch. Both global and myeloid-specific deletion of 14-3-3[epsilon] resulted in exacerbated inflammatory arthritis and counteracted the protective effects of progranulin-mediated TNFR2 activation against inflammation and autoimmunity. TNFR2/14-3-3[epsilon] signaled through PI3K/Akt/mTOR to restrict NF-[kappa]B activation while simultaneously stimulating C/EBP[beta] activation, thereby instructing macrophage plasticity. Collectively, this study identifies 14-3-3[epsilon] as a previously unrecognized vital component of the TNFR2 receptor complex and provides new insights into the TNFR2 signaling, particularly its role in macrophage polarization with therapeutic implications for various inflammatory and autoimmune diseases with activation of the TNFR2/14-3-3[epsilon] antiinflammatory pathway., Introduction Rheumatoid arthritis (RA) is a common chronic autoimmune condition characterized by inflammatory joint disease (1), resulting from protracted inflammation of the synovial membrane. Macrophages are a major subset of [...]