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Patent
Shionogi & Co. and National Cerebral And Cardiovascular Center | Date: 2016-09-20

A medicinal composition for suppressing or preventing the metastasis of a malignant tumor, the composition comprising, as an active ingredient, at least one kind of vasoprotective agent selected from the following (i) to (iv): (i) angiotensin II receptor antagonist, (ii) HMG-CoA reductase inhibitor, (iii) ghrelin or its derivative, and (iv) adrenomedullin or its derivative; or a pharmacologically acceptable salt thereof.


Patent
National Cerebral And Cardiovascular Center and Mitsubishi Group | Date: 2017-02-08

Provided are a novel medicament for suppressing or preventing the metastasis of a malignant tumor such as carcinoma, a novel treatment or prevention method for suppressing or preventing the metastasis of a malignant tumor, etc. The medicament comprises a non-peptidic angiotensin type 2 receptor agonist as an active ingredient. In the medicament, the non-peptidic angiotensin type 2 receptor agonist may be, for example, a sulfonyl malonamide compound. The medicament may be a medicament for use in combination with an anticancer agent and/or an antitumor agent.


Patent
Nihon Kohden and National Cerebral And Cardiovascular Center | Date: 2015-07-29

A monitoring apparatus includes a condition determining section which is configured to determine a condition of one of a heart, lungs, and blood vessels based on: a concentration of carbon dioxide in an expired gas which is measured by using a first sensor; and an oxygen transport parameter or a metabolic parameter which is measured by using a second sensor.


Patent
National Cerebral And Cardiovascular Center, Foundation For Biomedical Research And Innovation, Hyogo College of Medicine, Hokkaido University and Kaneka Corporation | Date: 2016-06-29

An object of the present invention is to provide a method for producing a mesenchymal stromal cell composition, comprising conveniently and aseptically separating high-purity amnion-derived MSCs by performing enzyme treatment only once. According to the present invention, the following are provided: a method for producing a mesenchymal stromal cell composition, comprising: performing enzyme treatment of an amnion with collagenase and thermolysin and/or dispase; and filtering the enzyme-treated amnion through a mesh; a method for producing a cryopreserved mesenchymal stromal cell composition; and a therapeutic agent comprising as an active ingredient the mesenchymal stromal cell composition for a disease selected from graft-versus-host disease, inflammatory bowel disease, systemic lupus erythematosus, liver cirrhosis, or radiation enteritis.


Provided are a peptide that enables surface treatment of a scaffold for tissue repair that makes it possible to accelerate the repair of living tissue without using a material that negatively affects the repair of living tissue, a complex containing this peptide, a scaffold for tissue repair surface treated using this peptide or this complex, a surface treatment method for a scaffold for tissue repair using this peptide or this complex, and a treatment solution or set of treatment solutions to be used in this surface treatment method. Surface treatment of a scaffold for tissue repair is conducted by combining glycosaminoglycan and a peptide containing adhesive sites and basic sites each comprising predetermined amino acid residues.


Patent
Seiko Epson Corporation and National Cerebral And Cardiovascular Center | Date: 2016-05-16

A first blood vessel diameter and a second blood vessel diameter are measured using a first ultrasonic probe and a second ultrasonic probe that are provided close to a blood vessel of a subject so as to be situated at a given distance (Lp). Characteristic phases of a pulse wave are determined from the peak of a second-order differential value of the first blood vessel diameter and the peak of a second-order differential value of the second blood vessel diameter, and the difference (t) in pulse wave transit time is calculated from the difference in timing between the characteristic phases to calculate pulse wave velocity (PWV). A given calculation process that uses the pulse wave velocity (PWV) and the measured blood vessel diameter as variables is performed to calculate blood pressure.


Anzai T.,National Cerebral and Cardiovascular Center
Circulation Journal | Year: 2013

After myocardial infarction (MI), inflammatory cells such as neutrophils, followed by monocytes and macrophages, infiltrate and phagocytose the necrotic tissues, as well as secreting a variety of inflammatory cytokines. The vulnerable myocardium, which consists of necrotic tissue and inflammatory cells, is susceptible to wall stress, resulting in infarct expansion. Subacute cardiac rupture is an extreme form of infarct expansion, whereas ventricular aneurysm is its chronic form and a trigger for subsequent left ventricular (LV) remodeling. Although post-infarction inflammation is essential for the healing process, excessive inflammation could play an important role in the development of LV remodeling. Increase in the C-reactive protein level, which reflects myocardial inflammation, is reported to be a useful predictive marker for cardiac rupture, ventricular aneurysm and LV remodeling. In addition, an increase in peripheral monocyte count is associated with a poor outcome after MI, and an animal study has demonstrated that granulocyte/macrophage-colony stimulating factor induction causes excessive macrophage infiltration in the infarcted area and worsening of LV remodeling. Recently, it was also found that dendritic cells play an important role in controlling excessive inflammation caused by monocytes/macrophages. Thus, inflammation that develops after MI is a doubleedged sword, and how to control inflammation to suppress pathological remodeling is an important issue to be considered in developing new treatment for heart failure.


Noguchi T.,National Cerebral and Cardiovascular Center
Journal of the American College of Cardiology | Year: 2011

The purpose of this study was to determine whether high-intensity carotid plaques visualized by a noncontrast T1-weighted imaging technique, magnetization-prepared rapid acquisition with gradient echo (MPRAGE), predict future coronary events in patients with clinically stable coronary artery disease (CAD). Coronary plaque vulnerability to rupture can be assessed by examining for the presence of atherosclerosis and measuring intima media thickness (IMT) in surrogate vessels such as the carotid arteries. We previously showed that MPRAGE successfully identifies vulnerable carotid plaques as high-intensity signals. It remains unclear, however, if the presence of carotid high-intensity plaques (HIP) is associated with an increased risk of coronary events. We examined the signal intensity of carotid plaques in 217 patients with clinically stable CAD using MPRAGE with magnetic resonance imaging and measured IMT with ultrasonography. A carotid HIP was defined as a signal >200% that of the adjacent muscle. All patients were divided into 2 groups according to the presence or absence of HIP, namely, the HIP group (n = 116) and the non-HIP group (n = 101), and were followed up for as long as 72 months. The presence of HIP was significantly associated with cardiac events compared to the non-HIP group (log-rank p < 0.0001). Furthermore, multivariate Cox regression analysis identified the presence of HIP as the strongest independent predictor of cardiac events (hazard ratio: 3.15; 95% confidence interval: 1.93 to 5.58, p < 0.0001) compared with IMT (hazard ratio: 1.62, 95% confidence interval: 0.97 to 2.44, p = 0.055) and other coronary risk factors. Characterization of carotid plaques using magnetic resonance imaging with MPRAGE provides more clinically relevant information for the risk assessment of CAD patients than IMT. Copyright © 2011 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.


Patent
National Cerebral And Cardiovascular Center | Date: 2016-07-06

The present invention provides a base material for forming a connective tissue structure which can accurately cut the connective tissue structure to a predetermined shape and a method for producing the connective tissue structure. A cutting-line forming groove (28) is formed in a surface of a base material (19). The base material (19) is placed under an environment in which a biological tissue material is present. A membranous connective tissue structure (20) is formed on the surface of the base material (19). At that time, a connective tissue (30) is made to invade into the cutting-line forming groove (28). A cutting line (31) for cutting is formed in the connective tissue structure (20). The connective tissue structure (20) is accurately cut along the cutting line (31) to a predetermined shape.


The present invention provides a membranous connective tissue-forming substrate on which a membranous connective tissue having a sufficient thickness and strength can be formed and a method for producing a membranous connective tissue by using the substrate. Specifically, a connective tissue-forming section 2 is provided on the surface of the substrate. The connective tissue-forming section 2 is surrounded by a thickness-increasing section 3 to enlarge a membranous connective tissue-forming substrate 1 as a whole. The membranous connective tissue-forming substrate 1 is placed under an environment in which a biological tissue material is present to form a membranous connective tissue on the surface of the substrate. In proportion as the size of the membranous connective tissue-forming substrate 1 increases, the thickness of the membranous connective tissue increases. A surplus portion formed on the surface of the thickness-increasing section 3 is removed from the connective tissue. A membranous connective tissue having an increased thickness and strength can be thus obtained.

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