124 research outputs found

    Ovalbumin-induced plasma interleukin-4 levels are reduced in ceramide kinase-deficient DO11.10 RAG1-/- mice

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    Ceramide kinase (CERK) produces the bioactive lipid ceramide-1-phosphate (C1P) and is a key regulator of ceramide and dihydroceramide levels. It is likely that CERK and C1P play a role in inflammatory processes but the cells involved and the mechanisms used remain to be clarified. In particular, the impact of CERK on T-cell biology has not been studied so far. Here, we used Cerk-/- mice backcrossed with DO11.10/RAG1-/- mice to probe the effect of CERK ablation on T-cell activation. Levels of interleukin (IL)-2, IL-4, IL-5, IL-13, of tumor necrosis factor (TNF)-α, and of interferon (INF)-γ were recorded following ovalbumin challenge in vivo and using ovalbumin-treated splenocytes ex- vivo. Absence of CERK led to a significant decrease in the production of IL-4, thus suggesting that CERK may polarize T cells towards the TH2 cell subtype. However, the importance of CERK to TH2 cell biology will have to be investigated further because in a model of asthma, which is TH2-cell driven, Cerk-/- mice responded like wild-type animals

    Spermatic Cord Lymphoma: A Case Report and Literature Review

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    Spermatic cord lymphoma is a rare lethal disease. It has a poor prognosis even in stage I or II disease when treated locally, therefore, multidisciplinary treatment for early stage is recommended. On the other hand, the treatment of choice for stage III or IV spermatic cord lymphoma remains to be determined. It is said that spermatic cord lymphoma is clinicopathologically similar to primary testicular lymphoma, therefore the treatment of spermatic cord lymphoma has often been determined by reference to the recommended treatment for primary testicular lymphoma. Here we report a new case of spermatic cord lymphoma, which was found in stage IV disease. We also review thirty-three cases which have been reported as spermatic cord lymphoma to date, and discuss treatment options

    Material properties of a low contraction and resistivity silicon-aluminum composite for cryogenic detectors

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    We report on the cryogenic properties of a low-contraction silicon-aluminum composite, namely Japan Fine Ceramics SA001, to use as a packaging structure for cryogenic silicon devices. SA001 is a silicon--aluminum composite material (75% silicon by volume) and has a low thermal expansion coefficient (\sim1/3 that of aluminum). The superconducting transition temperature of SA001 is measured to be 1.18 K, which is in agreement with that of pure aluminum, and is thus available as a superconducting magnetic shield material. The residual resistivity of SA001 is 0.065 μΩm\mathrm{\mu \Omega m}, which is considerably lower than an equivalent silicon--aluminum composite material. The measured thermal contraction of SA001 immersed in liquid nitrogen is L293KL77KL293K=0.12\frac{L_{293\mathrm{K}}-L_{77\mathrm{K}}}{L_{293\mathrm{K}}}=0.12%, which is consistent with the expected rate obtained from the volume-weighted mean of the contractions of silicon and aluminum. The machinability of SA001 is also confirmed with a demonstrated fabrication of a conical feedhorn array, with a wall thickness of 100 μm\mathrm{\mu m}. These properties are suitable for packaging applications for large-format superconducting detector devices.Comment: 8 pages, 4 figures, 1 table, accepted for the Journal of Low Temperature Physics for the LTD19 special issu

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    レチノイドは細胞内の特異的レセプターと結合し,各種遺伝子の発現を調節することにより,細胞の分化,増殖および抗炎症作用など,種々の生理活性を示すことが多数報告されている。本研究では,これらの欠点を補うべく新しく合成されたレチノイド誘導体である,4-[(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthyl)carbamoyl]benzoic acid(Am-80)の免疫薬理学的作用について検討し,次いでその作用機序についても合わせて検討した。Am-80は,マウスの2,4-dinitrofluorobenzene(DNFB)誘発接触性皮膚炎およびハプテン特異的1gE産生が強く見られるDNFB反復塗布によるマウス接触性皮膚炎において,耳介の腫脹を用量依存的に強く抑制した。また,Am-80はin vitroでの単核球からの抗原によるinterleukin-6(IL-6)ならびにinterferon-γ(IFN一γ)産生を抑制し,その抑制は転写レベルにおいて観察された。Am-80は,マウスのtypeIIコラーゲン誘発関節炎の発症を抑制し,C.Paruvum 前処置マウスのLipopolysaccharide(LPS)によるIL-6産生を抑制したが,ConcanavarinA(ConA)刺激したT細胞からのIFN-γおよびinteleukin-4(IL-4)産生には影響を及ぼさなかった。さらにAm-80は,ラットの実験的アレルギー性脳脊髄炎(EAE)の臨床症状および脊髄への細胞浸潤を用量依存的に抑制したが,投与中止によりEAEの再発が観察された。また,脊髄におけるIL-6mRNAの発現レベルにおいても同様に,投与中止後のIL-6mRNAの発現上昇が観察された。以上の結果から,Am-80は,リンパ球以外の細胞からのIL-6およびIFN-γの産生を選択的に抑制することにより,マウスおよびラットの接触性皮膚炎ならびに自己免疫疾患発症を抑制することが示唆された。これらの知見は,免疫性疾患における炎症性サイトカインの重要性ならびにレチノィド誘導体の治療薬としての有用性を示唆するものである。Retinoids have been reported to elicit a variety of biological activities such as cell differentiation, cell growth and anti-inflammatory effect, through the binding with specific intracellular receptors. In this study, we examined immunopharmacological effects of 4-[(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthyl) carbamoyl]benzoic acid (Am-80), a new retinoid-derivative, and its mechanism of actions. Am-80 inhibited ear swelling in a dose-dependent manner on 2,4-dinitrofluorobenzene (DNFB)-induced contact dermatitis and on contact dermatitis by the repeated applications of DNFB in mice. In addition, Am-80 inhibited production of inteleukin-6 (IL-6) and interferon-γ (IFN-γ) on mononuclear cells in vitro, and its inhibition was observed on a transcriptional level. Am-80 inhibited the elicitation of type II collagen-induced arthritis in mice. Am-80 inhibited lipopolysaccharide (LPS)-induced IL-6 production in C. Parvum-pretreated mice, but not the production of IFN-γ or IL-4 in T cells stimulated with concanavarin A (Con A) in vitro. Am-80 diminished clinical symptoms and infiltration of inflammatory cells into the spinal code on experimental allergic encephalomyelitis (EAE)-induced rats. However, after stopping administration, EAE recurred in DA rats treated with AM-80. Furthermore, the expressional level of IL-6 mRNA was diminished during the administration of Am-80,but provoked as soon as it was stopped. Therefore, Am-80 cured mice contact dermatitis, arthritis and rat EAE through the selective inhibition of IL-6 and IFN-γ secreted from inflammatory cells except for T cells. This evidence may suggest the importance of inflammatory cytokines and the usefulness of retinoid derivatives in immune disorders
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