46 research outputs found

    2D-Time of Flight MR Angiography in Intrathoracic Masses

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    正常ボランティア5例, 胸部腫瘤性病変の患者15例に対してMR Angiographyを施行した.MRAは, 6秒の息、止めでFLASH法(TR=20msec, TE=8msec, Flip angle=30°)を用いて撮像した像から作成した.全ての症例で胸部大動脈, 上大静脈, 下大静脈, 肺動脈及び肺静脈根部など太い血管の明瞭なMRA像が得られ, 腫瘤とそれら大血管系との関係が把握しやすく胸部腫瘤性病変の評価に有用と考えられた.MR Angiography of the thorax was performed in 5 healthy volunteers and 15 patients with intrathoracic masses. 2D-MRA was obtained sequentially by means of a fast low angle shot(FLASH)technique(TR=20msec.TE=8msec, Flip angle=30within a 6-second period of breath holding. MRA for great vessels was successfully completed in all volunteers and all patients. The relation between tumor and vasculature can be visualized so definitely that MRA may be thought to be a promising complement to MR imaging in the evaluation of intrathoracic masses

    Reconstitution of amoeboid motility in vitro identifies a motor-independent mechanism for cell body retraction

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    Author Posting. © The Author(s), 2011. This is the author's version of the work. It is posted here by permission of Elsevier B.V. for personal use, not for redistribution. The definitive version was published in Current Biology 21 (2011): 1727-1731, doi:10.1016/j.cub.2011.08.047.Crawling movement in eukaryotic cells requires coordination of leading edge protrusion with cell body retraction [1-3]. Protrusion is driven by actin polymerization along the leading edge [4]. The mechanism of retraction is less clear; myosin contractility may be involved in some cells [5] but is not essential in others [6-9]. In Ascaris sperm, protrusion and retraction are powered by the major sperm protein (MSP) motility system instead of the conventional actin apparatus [10-11]. These cells lack motor proteins [12] and so are well-suited to explore motor-independent mechanisms of retraction. We reconstituted protrusion and retraction simultaneously in MSP filament meshworks, called fibers, that assemble behind plasma membrane-derived vesicles. Retraction is triggered by depolymerization of complete filaments in the rear of the fiber [13]. The surviving filaments reorganize to maintain their packing density. By packing fewer filaments into a smaller volume the depolymerizing network shrinks and thereby generates sufficient force to move an attached load. Thus, this work provides direct evidence for motorindependent retraction in the reconstituted MSP motility system of nematode sperm. This mechanism could also apply to actin-based cells and may explain reports of cells that crawl even when their myosin activity is compromised.This work was supported by the National Institutes of Health (R37-GM29994). N.N. was supported by an NIH grant (R01-EB002583) to Rudolf Oldenbourg

    Five-year quality of life assessment after carbon ion radiotherapy for prostate cancer

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    The aim of this study was to prospectively assess 5-year health-related quality of life (HRQOL) of patients treated with carbon ion radiotherapy (C-ion RT) for clinically localized prostate cancer. A total of 417 patients received carbon ion radiotherapy at a total dose of 63–66 Gray-equivalents (GyE) in 20 fractions over 5 weeks, and neoadjuvant and adjuvant androgen deprivation therapy (ADT) were administered for intermediate and high-risk patients. A HRQOL assessment was performed at five time points (immediately before the initiation of C-ion RT, immediately after, and at 12, 36 and 60 months after completion of C-ion RT) using Functional Assessment of Cancer Therapy (FACT) questionnaires. FACT-G and FACT-P scores were significantly decreased; however, the absolute change after 60 months was minimal. The transient decreases in the Trial Outcome Index (TOI) score returned to their baseline levels. Use of ADT, presence of adverse events, and biochemical failure were related to lower scores. Scores of subdomains of FACT instruments indicated characteristic changes. The pattern of HRQOL change after C-ion RT was similar to that of other modalities. Further controlled studies focusing on a HRQOL in patients with prostate cancer are warranted

    Mamld1 Knockdown Reduces Testosterone Production and Cyp17a1 Expression in Mouse Leydig Tumor Cells

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    MAMLD1 is known to be a causative gene for hypospadias. Although previous studies have indicated that MAMLD1 mutations result in hypospadias primarily because of compromised testosterone production around the critical period for fetal sex development, the underlying mechanism(s) remains to be clarified. Furthermore, although functional studies have indicated a transactivation function of MAMLD1 for the non-canonical Notch target Hes3, its relevance to testosterone production remains unknown. To examine these matters, we performed Mamld1 knockdown experiments.Mamld1 knockdown was performed with two siRNAs, using mouse Leydig tumor cells (MLTCs). Mamld1 knockdown did not influence the concentrations of pregnenolone and progesterone but significantly reduced those of 17-OH pregnenolone, 17-OH progesterone, dehydroepiandrosterone, androstenedione, and testosterone in the culture media. Furthermore, Mamld1 knockdown significantly decreased Cyp17a1 expression, but did not affect expressions of other genes involved in testosterone biosynthesis as well as in insulin-like 3 production. Hes3 expression was not significantly altered. In addition, while 47 genes were significantly up-regulated (fold change >2.0×) and 38 genes were significantly down-regulated (fold change <0.5×), none of them was known to be involved in testosterone production. Cell proliferation analysis revealed no evidence for compromised proliferation of siRNA-transfected MLTCs.The results, in conjunction with the previous data, imply that Mamld1 enhances Cyp17a1 expression primarily in Leydig cells and permit to produce a sufficient amount of testosterone for male sex development, independently of the Hes3-related non-canonical Notch signaling

    Effect of spinal fusion on joint space narrowing of the hip: comparison among non-fusion, short fusion, and middle or long fusion

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    Abstract Background Lumbar fusion corrects spinal deformities and improves spinal complications. Hip osteoarthritis (OA) is strongly correlated with spinal mobility, and joint space narrowing of the hip after spinal fusion has gained attention. This study aimed to elucidate the effect of spinal fusion on hip joint space narrowing. Materials and methods We retrospectively examined 530 hips of 270 patients who underwent spinal surgery. All the patients underwent whole-spine radiography before and at the final follow-up. Patients were divided into three groups (N group: non-spinal fusion, S group: up to three interbody fusions, and L group: more than four interbody fusions). The rates of joint space narrowing, spinal parameters (sagittal vertical axis, thoracic kyphosis, lumbar lordosis, sacral slope, pelvic tilt, and pelvic incidence), and limb length discrepancy at the final follow-up were compared. A multilinear regression analysis was performed to identify the risk factors for the rate of joint space narrowing. Results The rate of joint space narrowing was significantly higher in the L group than in the N and S groups (P < 0.001). No significant difference in the rate of joint space narrowing was observed between the N and S groups. Multiple linear regression analysis revealed that the number of fusion levels (p < 0.05) and follow-up period (p < 0.001) were independent risk factors for joint space narrowing. Spinal parameters at the final follow-up were not independent risk factors. Conclusions Long spinal fusion (more than four levels) led to significantly greater joint space narrowing of the hip than short (up to three levels) or no fusion. Spinal alignment did not affect joint space narrowing of the hip. Surgeons should be aware that more than four interbody fusions may result in worse joint space narrowing of the hip. Level of evidence IV, retrospective stud
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