Effects of laser wavelength and density scalelength on absorption of ultrashort intense lasers on solid-density targets

Hot electron temperatures and electron energy spectra in the course of interaction between intense laser pulse and overdense plasmas are reexamined from a viewpoint of the difference in laser wavelength. The hot electron temperature measured by a particle-in-cell simulation is scaled by $I$ rather than $I \lambda^2$ at the interaction with overdense plasmas with fixed ions, where $I$ and $\lambda$ are the laser intensity and wavelength, respectively.Comment: 12th International Congress on Plasma Physics, 25-29 October 2004, Nice (France

Targeting TNF-α suppresses the production of MMP-9 in human salivary gland cells

Objective: Tumor necrosis factor-α (TNF-α) is a pleiotropic cytokine that plays an essential role in inflammation and apoptosis. Our previous study suggested that TNF-α-induced activation of matrix metalloproteinase-9 (MMP-9) resulted in the destruction of acinar tissue in the salivary glands of patients with Sjögren’s syndrome (SS) via disruption of the acinar cell-basement membrane. Recently, a wide array of biological agents has been designed to inhibit TNF, including etanercept and adalimumab. In this study, we demonstrate the suppressive effect of anti-TNF agents on TNF-α-induced MMP-9 production in NS-AV-AC, an immortalized human salivary gland acinar cell line. Materials and Methods: NS-AV-AC cells were treated with etanercept or adalimumab after TNF-α treatment. MMP-9 production and enzymatic activity were, respectively, visualized by real-time PCR and ELISA assay, and evaluated by gelatin zymography, and apoptosis was evaluated by DNA fragmentation assay. Results: TNF-α induced the production of MMP-9 in NS-SV-AC cells. However, this production was greatly inhibited by treatment with etanercept or adalimumab. In addition, TNF-α-induced DNA fragmentation was prevented by treatment with etanercept or adalimumab. Conclusions: These results may indicate that anti-TNF agents would have therapeutic efficacy for preventing destruction of the acinar structure in the salivary glands of patients with SS

チホウ ジチタイ ノ ブンカ シンコウ ホウセイ

研究ノー

Laser Powder-Bed Fusion as an Alloy Development Tool: Parameter Selection for In-Situ Alloying Using Elemental Powders

The design of advanced alloys specifically tailored to additive manufacturing processes is a research field that is attracting ever-increasing attention. Laser powder-bed fusion (LPBF) commonly uses pre-alloyed, fine powders (diameter usually 15–45 µm) to produce fully dense metallic parts. The availability of such fine, pre-alloyed powders reduces the iteration speed of alloy development for LPBF and renders it quite costly. Here, we overcome these drawbacks by performing in-situ alloying in LPBF starting with pure elemental powder mixtures avoiding the use of costly pre-alloyed powders. Pure iron, chromium, and nickel powder mixtures were used to perform in-situ alloying to manufacture 304 L stainless steel cube-shaped samples. Process parameters including scanning speed, laser power, beam diameter, and layer thickness were varied aiming at obtaining a chemically homogeneous alloy. The scientific questions focused on in this work are: which process parameters are required for producing such samples (in part already known in the state of the art), and why are these parameters conducive to homogeneity? Analytical modelling of the melt pool geometry and temperature field suggests that the residence time in the liquid state is the most important parameter controlling the chemical homogeneity of the parts. Results show that in-situ alloying can be successfully employed to enable faster and cost-efficient rapid alloy development

Role of CXCL10 in pathogenesis of Sjögren's syndrome

Sjögren's syndrome (SS) is a common autoimmune disease characterized by the destruction of acinar structure by marked lymphocytic infiltrates in the salivary and lacrimal glands, resulting in sicca symptoms. Gene expression profiling of lip salivary glands (LSGs) shows that C-X-C motif chemokine 10 (CXCL10) expression is upregulated in patients with primary SS (pSS). CXCL10 and its receptor, C-X-C receptor 3 (CXCR3), contribute to the pathogenesis of SS. We investigated the clinical significance of CXCL10 and CXCR3 in the autoimmune lesions of pSS and the molecular mechanisms of CXCL10 upregulation in the salivary gland cells. CXCL10 showed particularly intense staining in LSG ductal cells from pSS patients. CXCR3 expression was detected primarily in CD163+ macrophages. The number of CXCR3+CD163+ macrophages was inversely correlated with the severity of LSG inflammatory lesions. Our in vitro experiments demonstrated that human salivary gland ductal (NS-SV-DC) cells produced higher levels of CXCL10 than acinar (NS-SV-AC) cells. Furthermore, NS-SV-DC and NS-SV-AC cells had different regulators of CXCL10 enhancement: interferon (IFN)-γ had more potential than IFN-α, tumor necrosis factor (TNF)-α, and interleukin (IL)1-β in the induction of CXCL10 production in NS-SV-DC cells, whereas TNF-α had the potential to induce CXCL10 production in NS-SV-AC cells. Our results suggest that CXCL10 overexpression in salivary glands is mainly caused by IFN-γ-stimulated salivary gland ductal cells. The enhanced production of CXCL10 by ductal cell IFN-γ results in the migration of CXCR3+ immune cells. CXCL10 plays an important role in SS pathogenesis, and CXCL10 regulation may be useful in the treatment of SS patients

ビスコクラウリン型アルカロイドであるセファランチンは、1次性シェーグレン症候群患者の唾液分泌量を著明に増加させる

Objective: Our previous findings suggested that the suppression of tumor necrosis factoralpha (TNF-α)-induced matrix metalloproteinase (MMP)-9 production by the biscoclaurine alkaloid cepharanthine could prevent the destruction of the acinar structure in the salivary glands of murine Sjögren's syndrome. Here, we examined the effect of cepharanthine on the salivary secretion in primary Sjögren's syndrome (pSS) patients. Methods: In this single-center, open-label pilot study, 29 patients with pSS (28 women, 1 man) received 6 mg/day orally cepharanthine for 12 months. Standard clinical assessments and stimulated salivary flow were examined at baseline and each month for 12 months in all 29 patients. In eight of the patients, inflammatory lesions in the salivary glands were histologically investigated before and after the cepharanthine treatment. We analyzed the expressions of p65, phosphorylated IκB-α, MMP-9, and type IV collagen immunohistochemically. Results: All patients completed the study without any adverse events. A significant increase in salivary flow was observed after the cepharanthine treatment compared to baseline. The serological analysis revealed that the 14 patients with an anti-Sjögren's-syndrome-related antigen A (anti-SSA/Ro) antibody value that was either negative or 64 U/ml did not. The immunohistochemical analysis demonstrated that although p65, phosphorylated IκB-α, and MMP-9 were more strongly stained in the acinar cells of the patients at baseline compared to the staining at the completion of cepharanthine treatment, the continuity of type IV collagen was observed following the cepharanthine treatment. These results indicate that cepharanthine could inhibit the phosphorylation of IκB-α, followed by the prevention of MMP-9 activation and the stabilization of type IV collagen. Conclusions: Our findings suggest that cepharanthine could be a promising agent for improving salivary secretion in pSS patients

ニューラルネットワークを用いた動画像認識技術の生態系保全への適用について

要約のみTohoku University千葉聡課