142 research outputs found

    A Proposal for Analysis and Prediction for Software Projects using Collaborative Filtering, In-Process Measurements and a Benchmarks Database

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    PROCEEDINGS OF THE INTERNATIONAL CONFERENCE ON SOFTWARE PROCESS AND PRODUCT MEASUREMENT(MENSURA 2006)CÁDIZ – SPAINNOVEMBER, 6 – 8, 2006Alain Abran Reiner Dumke Mercedes Ruiz (Eds.)刊行年月日は会議開催日を参考にし

    Papillary glioneuronal tumor growing slowly for 26 years: illustrative case

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    BACKGROUND: Papillary glioneuronal tumors (PGNTs) are classified as a type of World Health Organization grade I mixed neuronal-glial tumor. Most PGNTs involve cystic formations with mural nodules and solid components in the cerebral hemispheres, and PGNTs occur mainly in young adults. The long-term prognosis of PGNTs remains unclear. OBSERVATIONS: A 38-year-old male had been diagnosed with an arachnoid cyst associated with epilepsy in a local hospital. The initial magnetic resonance imaging (MRI) study showed the tumor as a heterogeneously enhanced nodule in the left postcentral gyrus. Subsequent MRI studies showed slow growth of the tumor for 26 years. He underwent gross total resection to control his epilepsy. The histopathological findings revealed pseudopapillary structures involving hyalinized blood vessels with a single or pseudostratified layer of cuboidal glial cells with round nuclei and scant cytoplasm. At the periphery of the lesion, Rosenthal fibers and acidophilic granule bodies were observed in the gliotic brain tissue. Immunohistochemically, some interpapillary cells were positive for NeuN. On the basis of these findings, the tumor was diagnosed as a PGNT. LESSONS: This PGNT showed slow growth for 26 years. When recognizing a slowly growing tumor in the cerebral hemispheres of relatively young people that is associated with epileptic seizures, PGNT should be considered as a differential diagnosis

    Preoperative obliteration of choroidal arteries in the treatment of large hypervascular tumors in the lateral ventricle

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    BACKGROUND: Removal of large hypervascular tumors in the lateral ventricle still poses a surgical challenge. These tumors are usually fed from choroidal arteries, and vascular control is typically performed late during the removal. We aimed to evaluate the clinical efficacy of our strategy for persistent preoperative obliteration of feeders from the choroidal arteries to manage large hypervascular tumors in the lateral ventricle. METHODS: We retrospectively analyzed six patients with hypervascular tumors in the lateral ventricle. We first attempted to obstruct feeders using endovascular treatment, and, if unavailable, performed initial microsurgical occlusion through the temporal horn for the staged tumor removal. RESULTS: In all patients, feeder obliteration was successfully performed; the anterior choroidal arteries were occluded by the endovascular treatment and microsurgical occlusion in one and five patients, respectively, while the lateral posterior choroidal arteries were occluded via endovascular treatment in four patients. No patients had permanent symptoms due to feeder obliteration, and tumor devascularization was achieved at the mean rate of 69.9%. During the tumor removal, the mean blood loss volume was 253 ml. No postoperative hemorrhage had occurred, and all patients scored ≤ 2 on the modified Rankin Scale at six months post-removal. CONCLUSIONS: Although further studies are warranted, persistent feeder obliteration of choroidal arteries could be an effective treatment strategy against large hypervascular tumors in the lateral ventricle

    A Patient With Thiamine Deficiency Exhibiting Muscle Edema Suggested by MRI

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    Myalgia is sometimes observed in patients with thiamine-deficiency neuropathy. However, the detailed mechanism(s) underlying muscular manifestations have been poorly elucidated. We herein report a possible patient with thiamine-deficiency neuropathy exhibiting muscle weakness and myalgia in lower limbs. The patient exhibited abnormal muscle signal intensities on MRI corresponding to the site of myalgia. After thiamine replacement therapy, rapid improvement of clinical symptoms and abnormal MRI findings were observed. Muscle MRI findings in this case implicated the possible mechanism of myalgia observed in patients with thiamine deficiency neuropathy

    27ヒドロキシコレステロールはエストロゲン受容体を介してヒトSLC22A12の発現を制御する

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    The excretion and reabsorption of uric acid both to and from urine are tightly regulated by uric acid transporters. Metabolic syndrome conditions, such as obesity, hypercholesterolemia, and insulin resistance, are believed to regulate the expression of uric acid transporters and decrease the excretion of uric acid. However, the mechanisms driving cholesterol impacts on uric acid transporters have been unknown. Here, we show that cholesterol metabolite 27-hydroxycholesterol (27HC) upregulates the uric acid reabsorption transporter URAT1 encoded by SLC22A12 via estrogen receptors (ER). Transcriptional motif analysis showed that the SLC22A12 gene promoter has more estrogen response elements (EREs) than other uric acid reabsorption transporters such as SLC22A11 and SLC22A13, and 27HC-activated SLC22A12 gene promoter via ER through EREs. Furthermore, 27HC increased SLC22A12 gene expression in human kidney organoids. Our results suggest that in hypercholesterolemic conditions, elevated levels of 27HC derived from cholesterol induce URAT1/SLC22A12 expression to increase uric acid reabsorption, and thereby, could increase serum uric acid levels.博士(医学)・甲第772号・令和3年3月15日© 2020 The Authors. The FASEB Journal published by Wiley Periodicals LLC on behalf of Federation of American Societies for Experimental Biology. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License(https://creativecommons.org/licenses/by-nc/4.0/), which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes
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