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991.
Hirashima Y Doshi M Hayashi N Endo S Akazawa Y Shichiri M Yoshida Y 《Neurosurgery》2012,70(3):602-609
992.
Kiyoko Kaneko Riei Kobayashi Makoto Yasuda Yoko Izumi Tomoyo Yamanobe Toru Shimizu 《International journal of urology》2012,19(8):765-772
Objectives: To analyze the crystal components and matrix proteins of urinary stones by proteomic analysis using liquid chromatography–tandem mass spectrometry. Methods: Urinary stones were obtained from patients with gout and hyperuricemia. The outside and inside of the stones were measured non‐destructively with a micro area X‐ray diffractometer. After stones were powdered, extracted proteins were analyzed by proteomic analysis. Results: Of 17 investigated stones, seven were composed of calcium oxalate monohydrate or calcium oxalate dihydrate, seven were of uric acid, and three were a mixture of calcium oxalate monohydrate and uric acid. In calcium oxalate monohydrate or calcium oxalate dihydrate stones, osteopontin, uromodulin, albumin, protein Z, prothrombin, protein S, hemoglobin and histone H4 were identified. In uric acid stones, uromodulin, albumin, hemoglobin, calgranulins and immunoglobin G fragments were detected. Mixed stones of calcium oxalate monohydrate and uric acid contained both Ca‐binding proteins and abundant proteins. Matrix proteins were different when the crystal components of the stone were different, even when from the same patient. Conclusions: Proteins, such as uromodulin and albumin, are often detected in stones, regardless of crystal components. However, osteopontin, prothrombin, protein S and protein Z are identified specifically in calcium oxalate stones. Furthermore, immunoglobin G fragments are detected in uric acid stones. The role of these specific proteins in the different types of stones can be of particular interest. 相似文献
993.
Systemic lupus erythematosus (SLE) is a devastating autoimmune disease characterized by chronic inflammation and systemic destruction of host organs or tissue. A key feature of SLE is T cell dysfunction characterized by hyperresponsive antigen receptor signaling. In this issue of the JCI, McDonald and colleagues provide evidence that homeostasis of a subset of lipids, the glycosphingolipids (GSLs), is severely perturbed in the membranes of T cells from SLE patients. Furthermore, normalization of GSLs restored TCR signaling and ameliorated T cell dysfunction. These data suggest that targeting host metabolism may be an effective means of reinforcing self-tolerance and attenuating autoimmunity.
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by immune hyperactivity and loss of immunologic tolerance to self-antigens. Clinical manifestations often include symptoms of chronic inflammation, such as fatigue and fevers, as well as more specific features, including skin rashes, renal disease, arthritis, cardiovascular disease, vasculopathies, coagulopathies, and CNS involvement. The etiology of SLE is not well understood and likely includes both environmental and genetic factors. However, it is clear that dysfunction of multiple facets of host immunity underlies SLE pathogenesis, resulting in inflammatory immune cell infiltrates, autoantibody production, and deposition of pathogenic antibodies in target organs (reviewed in ref. 1). 相似文献
994.
Ziad A. Ali Vinicio de Jesus Perez Ke Yuan Mark Orcholski Stephen Pan Wei Qi Gaurav Chopra Christopher Adams Yoko Kojima Nicholas J. Leeper Xiumei Qu Kathia Zaleta-Rivera Kimihiko Kato Yoshiji Yamada Mitsutoshi Oguri Allan Kuchinsky Stanley L. Hazen J. Wouter Jukema Santhi K. Ganesh Elizabeth G. Nabel Keith Channon Martin B. Leon Alain Charest Thomas Quertermous Euan A. Ashley 《The Journal of clinical investigation》2014,124(12):5159-5174
Angioplasty and stenting is the primary treatment for flow-limiting atherosclerosis;
however, this strategy is limited by pathological vascular remodeling. Using a systems
approach, we identified a role for the network hub gene glutathione peroxidase-1
(GPX1) in pathological remodeling following human blood vessel
stenting. Constitutive deletion of Gpx1 in atherosclerotic mice
recapitulated this phenotype of increased vascular smooth muscle cell (VSMC) proliferation
and plaque formation. In an independent patient cohort, gene variant pair analysis
identified an interaction of GPX1 with the orphan protooncogene receptor
tyrosine kinase ROS1. A meta-analysis of the only genome-wide association
studies of human neointima-induced in-stent stenosis confirmed the association of the
ROS1 variant with pathological remodeling. Decreased GPX1 expression in
atherosclerotic mice led to reductive stress via a time-dependent increase in glutathione,
corresponding to phosphorylation of the ROS1 kinase activation site Y2274. Loss of
GPX1 function was associated with both oxidative and reductive stress,
the latter driving ROS1 activity via s-glutathiolation of critical
residues of the ROS1 tyrosine phosphatase SHP-2. ROS1 inhibition with crizotinib and
deglutathiolation of SHP-2 abolished GPX1-mediated increases in VSMC proliferation while
leaving endothelialization intact. Our results indicate that GPX1-dependent alterations in
oxido-reductive stress promote ROS1 activation and mediate vascular remodeling. 相似文献
995.
Atsushi Iwata Yoko Watanabe Naomichi Kumagai Maria Katafuchi-Nagashima Keita Sugiura Radhakrishnan Pillai Yoshiyuki Tatsumi 《Antimicrobial agents and chemotherapy》2014,58(8):4920-4922
Efinaconazole is a novel triazole antifungal drug for the topical treatment of onychomycosis, a nail infection caused mainly by dermatophytes. We assessed the potential of efinaconazole to induce resistance in dermatophytes by continuous exposure of Trichophyton rubrum strains to efinaconazole in vitro (12 passages) and in a guinea pig onychomycosis model (8 weeks). There was no evidence of efinaconazole resistance development in the tested strains under the experimental conditions used. 相似文献
996.
997.
Dr Yoshifumi Ubara Tetsuo Tagami Tatsuya Suwabe Yoko Sogawa Junichi Hoshino Yasushi Higa 《Amyloid》2013,20(3):178-183
We report autopsy findings in an 83-year-old woman with myeloperoxidase-type anti-neutrophil cytoplasmic antibody (MPO-ANCA)-positive microscopic polyangiitis and systemic AA amyloidosis. With a diagnosis of MPO-ANCA-related microscopic polyangiitis, the patient was treated with corticosteroids, but she died of intractable enteritis. Autopsy showed inactive vasculitis affecting small arteries in kidney, lung, intestinal tract, and skeletal muscle. Gastrointestinal viscera were thickened, and AA-amyloid was demonstrated in arterioles and surrounding tissues. Amyloidosis also involved heart, kidney, gallbladder, pancreas, salivary gland, and subcutis. ANCA-positive microscopic polyangiitis appears to have been the likely cause of this patient's AA-amyloidosis. 相似文献
998.
999.
Masanori Atsukawa Akihito Tsubota Noritomo Shimada Chisa Kondo Norio Itokawa Ai Nakagawa Satomi Hashimoto Takeshi Fukuda Yoko Matsushita Hideko Kidokoro Yoshiyuki Narahara Katsuhisa Nakatsuka Katsuhiko Iwakiri Chiaki Kawamoto Choitsu Sakamoto 《Hepatitis monthly》2013,13(12)