735 research outputs found

    Induction and requirement of gene expression in the anterior cingulate cortex and medial prefrontal cortex for the consolidation of inhibitory avoidance memory

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    <p>Abstract</p> <p>Background</p> <p>Memory consolidation is a process to stabilize short-term memory, generating long-term memory. A critical biochemical feature of memory consolidation is a requirement for gene expression. Previous studies have shown that fear memories are consolidated through the activation of gene expression in the amygdala and hippocampus, indicating essential roles of these brain regions in memory formation. However, it is still poorly understood whether gene expression in brain regions other than the amygdala/hippocampus is required for the consolidation of fear memory; however, several brain regions are known to play modulatory roles in fear memory formation.</p> <p>Results</p> <p>To further understand the mechanisms underlying the formation of fear memory, we first identified brain regions where gene expression is activated after learning inhibitory avoidance (IA) by analyzing the expression of the immediately early genes c-fos and Arc as markers. Similarly with previous findings, the induction of c-fos and Arc expression was observed in the amygdala and hippocampus. Interestingly, we also observed the induction of c-fos and Arc expression in the medial prefrontal cortex (mPFC: prelimbic (PL) and infralimbic (IL) regions) and Arc expression in the anterior cingulate cortex (ACC). We next examined the roles of these brain regions in the consolidation of IA memory. Consistent with previous findings, inhibiting protein synthesis in the hippocampus blocked the consolidation of IA memory. More importantly, inhibition in the mPFC or ACC also blocked the formation of IA memory.</p> <p>Conclusion</p> <p>Our observations indicated that the formation of IA memory requires gene expression in the ACC and mPFC as well as in the amygdala and hippocampus, suggesting essential roles of the ACC and mPFC in IA memory formation.</p

    Effect of Lighting Using Yellow LEDs Designed for Moth Control on Flowering Response of Chrysanthemum

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    In order to develop a single light source which can be used both for moth control and flower inhibition in chrysanthemum, effects of blue (463nm), green (519nm), yellow green (576nm), yellow (597nm) and red light (646nm) LEDs on the flowering and the cut flower characteristics of chrysanthemum were investigated. As irradiance increased, the days to flower budding increased except under blue light. Yellow green and yellow LED had flower inhibiting effect equivalent to red LED. There was no difference in the crown bud number and the occurrence of abnormal flower irrespective of the light quality and irradiance. Next the, effects of night break and continuous lighting treatment by yellow LED on the flowering and cut flower characteristics of the chrysanthemum were investigated. There were significant differences in the cut flower characteristics except for the blade number on the neck in these treatments ; there was no practical problem with night break or continuous lighting. The minimum irradiance strength enough for flower inhibition in the continuous lighting treatment was about 80 mW m−2 that was half in night break treatment. Therefore, it is considered that yellow LED can be used as single light source for both moth control and flower inhibition in chrysanthemum.キクの防蛾と開花抑制に両用できる単一の光源を開発するために,青(ピーク波長:463nm),緑(519nm),黄緑(576nm),黄(597nm)および赤色(646nm)LED光が開花および切り花形質に及ぼす影響を調査した.青色光を除いて,放射照度が大きいほど発蕾までの日数が大きくなった.黄緑および黄色光は,赤色光とほぼ同等の開花抑制作用を有していた.いずれの光質および放射照度に関わらず,やなぎ葉数や花弁の展開異常の発生に差は見られなかった.次に,黄色LED光による暗期中断と終夜照明による影響を調査した.暗期中断と終夜照明では,やなぎ葉数を除く切り花形質に有意な差が見られたが,実用上の問題はなかった.開花抑制に必要となる放射照度の下限値は,終夜照明では約80mW m-2であり,暗期中断のほぼ半分であった.以上のことから,黄色LED光は,単一の光源としてキクの防蛾と開花抑制に両用することが可能であった

    Risk factors for lower limb lymphedema after lymph node dissection in patients with ovarian and uterine carcinoma

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    <p>Abstract</p> <p>Background</p> <p>Lymph node dissection has proven prognostic benefits for patients with ovarian or uterine carcinoma; however, one of the complications associated with this procedure is lymphedema. We aimed to identify the factors that are associated with the occurrence of lymphedema after lymph node dissection for the treatment of ovarian or uterine carcinoma.</p> <p>Methods</p> <p>A total of 694 patients with histologically confirmed ovarian (135 patients) or uterine cancer (258 with cervical cancer, 301 with endometrial cancer) who underwent lymph node dissection were studied retrospectively. Logistic regression analyses were used to identify the risk factors associated with occurrence of lymphedema.</p> <p>Results</p> <p>Among ovarian and uterine cancer patients who underwent pelvic lymph node dissection, post-operative radiotherapy (odds ratio: 1.79; 95% confidence interval: 1.20–2.67; p = 0.006) was statistically significantly associated with occurrence of lymphedema.</p> <p>Conclusion</p> <p>There was no relationship between any surgical procedure and occurrence of lymphedema among patients undergoing pelvic lymphadenectomy. Our findings are supported by a sound biological rationale because they suggest that limb lymphedema is caused by pelvic lymph node dissection.</p

    Usefulness of body surface mapping to differentiate patients with Brugada syndrome from patients with asymptomatic Brugada syndrome.

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    We attempted to determine the usefulness of body surface mapping (BSM) for differentiating patients with Brugada syndrome (BS) from patients with asymptomatic Brugada syndrome (ABS). Electrocardiograms (ECG) and BSM were recorded in 7 patients with BS and 35 patients with ABS. Following the administration of Ic antiarrhythmic drugs, BSM was recorded in 5 patients with BS and 16 patients with ABS. The maximum amplitudes at J0, J20, J40 and J60 were compared between the 2 groups, as were 3-dimensional maps. The maximum amplitudes at J0, J20 and J60 under control conditions were larger in patients with BS than in patients with ABS (P < 0.05). A three-dimensional map of the ST segments under control conditions in patients with BS showed a higher peak of ST elevation in the median precordium compared to that for patients with ABS. Increases in ST elevation at J20, J40 and J60 following drug administration were greater in patients with BS than in patients with ABS (P < 0.05). Evaluation of the change in amplitude of the ST segment at E5 caused by Ic drug administration was also useful for differentiating between the 2 groups. In conclusion, BSM was useful for differentiating patients with BS from those with ABS.</p

    盲ろう疑似体験を用いた障害理解と特殊教育教員養成カリキュラムへの応用に関する研究

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    金沢大学人間社会研究域学校教育系平成11年度における本研究は、前年度に引き続き、「盲ろう疑似体験」(以下、「疑似体験」)を中心に、まず次の各研究を行った(なお、実施した「疑似体験」は、前年度を含め9セッション、参加述べ人数は約300名である)。A.内外の関連文献の調査・分析、B.「疑似体験」実施上の技術的・基礎的諸条件について、C.「疑似体験」実施プログラムについて、D.「疑似体験」が内包する多様な側面と特徴について、の各研究である。さらに、今年度にあっては、10年度の研究実績やデータをもとに、これらの研究を継続・発展させるとともに、次の項目に関する研究に取り組んだ。 E.障害児者に関する知識・経験の量と質の異なる多様な参加者に対して「疑似体験」がもたらす効果の相違や限界について、F.特殊教育諸学校での教育実習に臨む学生への「疑似体験」の効果について、G.以上のような取り組みをもとに、「疑似体験」が重複障害に関する共感的な理解を深める可能性と特殊教育教員養成カリキュラムの一部に応用するうえでの実践的可能性にてついて、の各研究である。こうした取り組みの結果、AからEまでの項目については、一定の成果が得られた。しかし、FとGについては、いまだ成果は十分ではない。それは、「疑似体験」がほとんど一人ひとり異なる「内的体験」を参加者にもたらすために、一般化、マニュアル化が困難である、という構造的な課題を抱えているということが本研究をとおして明らかとなってきたからである。ただし、この間、各地の盲ろう者団体におけるセミナー、特殊教育、およびリハビリテーション、医療関係者等、専門職員を対象とする各種の研修会等で、本研究の成果を生かした「疑似体験」セッションが数多く実施され、筆者がこのうち複数のセミナーに直接貢献することができたことは小さくない成果だといえる。さらなる研究の継続の必要性を筆者は痛感している。研究課題/領域番号:10710118, 研究期間(年度):1998 – 1999出典:「盲ろう疑似体験を用いた障害理解と特殊教育教員養成カリキュラムへの応用に関する研究」研究成果報告書 課題番号10710118(KAKEN:科学研究費助成事業データベース(国立情報学研究所))(https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-10710118/)を加工して作

    Usefulness of acute pulmonary vasoreactivity test of sildenafil in treatment of portopulmonary hypertension. A case report

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    SummaryA 50-year-old man diagnosed with liver cirrhosis type C was referred to our hospital because of right heart failure with pulmonary hypertension. Echocardiography revealed enlargement of the right atrium and ventricle with severe tricuspid regurgitation. The peak flow velocity of tricuspid regurgitation by continuous wave Doppler echocardiography was 452cm/s. Right heart catheterization demonstrated severe pulmonary hypertension [pulmonary arterial pressure (PAP) systolic/diastolic/mean=73/20/41mmHg and pulmonary vascular resistance (PVR)=509dynscm–5] with portal hypertension. We diagnosed the patient as having portopulmonary hypertension (PoPH). Although we treated the patient with a prostacyclin analog, tricuspid regurgitation velocity was increased to 480cm/s four years after the start of the therapy. To select drugs for the treatment of PoPH, we performed an acute vasoreactivity test of sildenafil during right heart catheterization. Since single administration of sildenafil (20mg) decreased PAP (93/30/55–77/27/44mmHg) and PVR (908–833dynscm–5), we added sildenafil (20mg, t.i.d.) to the prostacyclin analog. Tricuspid regurgitation velocity decreased to 403cm/s one year after the addition of sildenafil. An acute vasoreactivity test of sildenafil during right heart catheterization was useful for the decision of the drug to be used in the treatment of PoPH

    CaMKIV over-expression boosts cortical 4-7 Hz oscillations during learning and 1-4 Hz delta oscillations during sleep

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    Mounting evidence suggests that neural oscillations are related to the learning and consolidation of newly formed memory in the mammalian brain. Four to seven Hertz (4-7 Hz) oscillations in the prefrontal cortex are also postulated to be involved in learning and attention processes. Additionally, slow delta oscillations (1-4 Hz) have been proposed to be involved in memory consolidation or even synaptic down scaling during sleep. The molecular mechanisms which link learning-related oscillations during wakefulness to sleep-related oscillations remain unknown. We show that increasing the expression of calcium/calmodulin dependent protein kinase IV (CaMKIV), a key nucleic protein kinase, selectively enhances 4-7.5 Hz oscillation power during trace fear learning and slow delta oscillations during subsequent sleep. These oscillations were found to be boosted in response to the trace fear paradigm and are likely to be localized to regions of the prefrontal cortex. Correlation analyses demonstrate that a proportion of the variance in 4-7.5 Hz oscillations, during fear conditioning, could account for some degree of learning and subsequent memory formation, while changes in slow delta power did not share this predictive strength. Our data emphasize the role of CaMKIV in controlling learning and sleep-related oscillations and suggest that oscillatory activity during wakefulness may be a relevant predictor of subsequent memory consolidation
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