392 research outputs found

    Altitudinal changes in Rubisco and APX activities in Aconogonum weyrichii in the alpine region of Mt. Fuji

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    o identify the determinants of the altitudinal distribution of an alpine herbaceous plant (Aconogonum weyrichii) from an eco-physiological viewpoint, we investigated the leaf characteristics concerned with photosynthetic capacity and tolerance of oxidative stress throughout this species altitude distribution on Mt. Fuji. Larger amounts of leaf nitrogen and Rubisco were found in populations growing at higher altitudes; however, initial activity of Rubisco did not increase with altitude in the summer, indicating that inactivation of Rubisco occurred in the higher populations. This inactivation would lead to a decrease in photosynthetic nitrogen use efficiency. When the leaves of A. weyrichii began to turn yellow in autumn, amounts of leaf nitrogen and Rubisco remarkably decreased in all populations throughout the altitude distribution. However, Rubisco activity in the higher populations did not decline until immediately before defoliation, suggesting that recovery from Rubisco inactivation occurred in these populations. The higher populations had a higher activity of APX than lower populations, contributing to maintaining Rubisco activity and photosynthetic production until the end of the growing period, which, in turn, are necessary for survival at higher altitudes

    Advantage of a precurved fenestrated endograft for aortic arch disease: Simplified arch aneurysm treatment in Japan 2010 and 2011

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    ObjectiveWe evaluated the results of our previous study investigating a precurved fenestrated endograft treatment for thoracic aortic aneurysms and aortic dissection extended to the aortic arch.MethodsFrom February 2010 to December 2011 at 35 Japanese centers, 383 patients (mean age, 75.7 ± 9.4 years) who required stent-graft landing in the aortic arch were treated with a precurved fenestrated endograft. The device has 19 3-dimensional curved stent skeleton types similar to aortic arch configurations and 8 graft fenestration types and is 24 to 44 mm in diameter and 16 to 20 cm long. The endografts were fabricated according to preoperative 3-dimensional computed tomographic images.ResultsTechnical and initial successes were achieved in 380 and 364 cases, respectively. Device proximal end was at zones 0 to 2 in 363, 15, and 2 patients, respectively. Lesions' proximal end ranged from zone 0 to 3 in 16, 125, 195, and 44 patients, respectively. The mean operative and fluoroscopic times were 161 ± 76 and 26 ± 13 min, respectively. The complications included stroke (7 patients), permanent paralysis (3), and perioperative death (6). No branch occlusion or proximal migration of the device occurred during follow-up.ConclusionsA precurved fenestrated endograft for endovascular repair in aortic arch disease rendered catheter manipulation simple and minimized operative complication risks. Although most patients had inadequate proximal landing zone and severely angled complex configuration, low mortality and morbidity and satisfactory clinical success were early outcomes, suggesting that this simplified treatment may be effective for aortic arch disease

    Non-invasive assessment of arterial stiffness using oscillometric blood pressure measurement

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    <p>Abstract</p> <p>Background</p> <p>Arterial stiffness is a major contributor to cardiovascular diseases. Because current methods of measuring arterial stiffness are technically demanding, the purpose of this study was to develop a simple method of evaluating arterial stiffness using oscillometric blood pressure measurement.</p> <p>Methods</p> <p>Blood pressure was conventionally measured in the left upper arm of 173 individuals using an inflatable cuff. Using the time series of occlusive cuff pressure and the amplitudes of pulse oscillations, we calculated local slopes of the curve between the decreasing cuff pressure and corresponding arterial volume. Whole pressure-volume curve was derived from numerical integration of the local slopes. The curve was fitted using an equation and we identified a numerical coefficient of the equation as an index of arterial stiffness (Arterial Pressure-volume Index, API). We also measured brachial-ankle (baPWV) PWV and carotid-femoral (cfPWV) PWV using a vascular testing device and compared the values with API. Furthermore, we assessed carotid arterial compliance using ultrasound images to compare with API.</p> <p>Results</p> <p>The slope of the calculated pressure-volume curve was steeper for compliant (low baPWV or cfPWV) than stiff (high baPWV or cfPWV) arteries. API was related to baPWV (<it>r </it>= -0.53, <it>P </it>< 0.05), cfPWV (<it>r </it>= -0.49, <it>P </it>< 0.05), and carotid arterial compliance (<it>r </it>= 0.32, <it>P </it>< 0.05). A stepwise multiple regression analysis demonstrated that baPWV and carotid arterial compliance were the independent determinants of API, and that API was the independent determinant of baPWV and carotid arterial compliance.</p> <p>Conclusions</p> <p>These results suggest that our method can simply and simultaneously evaluate arterial stiffness and blood pressure based on oscillometric measurements of blood pressure.</p

    Midkine as a factor to counteract the deposition of amyloid β-peptide plaques: in vitro analysis and examination in knockout mice

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    <p>Abstract</p> <p>Background</p> <p>Midkine is a heparin-binding cytokine involved in cell survival and various inflammatory processes. Midkine accumulates in senile plaques of patients with Alzheimer's disease, while it counteracts the cytotoxic effects of amyloid β-peptide and inhibits its oligomerization. The present study was conducted to understand the role of midkine upon plaque formation of amyloid β-peptide.</p> <p>Methods</p> <p>A surface plasmon assay was performed to determine the affinity of midkine for amyloid β-peptide. The deposition of amyloid β-peptide was compared in the brain of wild-type and midkine-deficient mice. An effect of midkine to microglias was examined by cell migration assay.</p> <p>Results</p> <p>Midkine bound to amyloid β-peptide with the affinity of 160 nM. The C-terminal half bound to the peptide more strongly than the N-terminal half, and heparin inhibited midkine from binding to the peptide. Pleiotrophin, which has about 50% sequence identity with midkine also bound to amyloid β-peptide. The deposition of amyloid β-peptide plaques in the cortex and hippocampus was more intense in 15-month-old midkine-deficient mice, compared to the corresponding wild-type mice. Midkine promoted migration of microglias in culture.</p> <p>Conclusions</p> <p>These results are consistent with the view that midkine attenuates the deposition of amyloid β-peptide plaques, and thus progression of Alzheimer's disease, by direct binding and also by promoting migration of microglias.</p
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