Nagasaki University | Date: 2017-02-08
The present invention aims to provide a novel compound for measuring cellular cytotoxicity or cell proliferation capacity accurately with high reproducibility, conveniently and rapidly, and a measurement method of cellular cytotoxicity or cell proliferation capacity by using the compound. The present invention relates to a compound represented by the formula (I):^(1) is a substituent, R^(2) and R^(3) are each an optionally substituted hydrocarbon group, or an optionally substituted heterocyclic group, Y is a substituent, n is an integer of 0 - 3, Z is a single bond, -O-, -S-, -SO-, -SO_(2)-, or -NR^(4)- (R^(4) is a hydrogen atom or a substituent), and A is an optionally substituted C_(1-6) alkylene group) or a salt thereof.
Luo L.,Nagasaki University
Circulation Research | Year: 2017
RATIONALE:: Stem cell therapy faces a number of challenges. It is difficult to grow, preserve, and transport stem cells before they are administered to the patient. Synthetic analogs for stem cells represent a new approach to overcome these hurdles and hold the potential to revolutionize regenerative medicine. OBJECTIVE:: We aim to fabricate synthetic analogs of stem cells and test their therapeutic potential for treatment of acute myocardial infarction in mice. METHODS AND RESULTS:: We packaged secreted factors from human bone marrow-derived mesenchymal stem cells (MSC) into Poly(lactic-co-glycolic acid) PLGA microparticles and then coated them with MSC membranes. We named these therapeutic particles “synthetic MSC” (or synMSC). synMSC exhibited a factor release profile and surface antigens similar to those of genuine MSC. synMSC promoted cardiomyocyte functions and displayed cryopreservation and lyophilization stability in vitro and in vivo. In a mouse model of acute myocardial infarction, direct injection of synMSC promoted angiogenesis and mitigated left ventricle remodeling. CONCLUSIONS:: We successfully fabricated a synMSC therapeutic particle and demonstrated its regenerative potential in mice with acute myocardial infarction. The synMSC strategy may provide novel insight into tissue engineering for treating multiple diseases. © 2017 American Heart Association, Inc.
News Article | March 27, 2017
Nocturia - a condition that makes people take numerous trips to the toilet at nighttime - may be caused by dietary habits, a new study has found. Researchers from the Nagasaki University in Japan have linked frequent nocturnal urination to a high sodium intake. Their conclusions, presented last weekend at the European Society of Urology congress in London, suggest the solution to this uncomfortable problem may be easily at hand. As study author Dr. Matsuo Tomohiro explains, "a simple dietary modification might significantly improve the quality of life for many people," who only need to cut back on salt consumption to avoid being glued to the toilet all night long. His study is the first to explore the connection between salt intake and the frequent need to use the bathroom, and additional research is needed to verify his findings. According to the National Sleep Foundation, nocturia is typically present in older people, affecting more than 50 percent of seniors over 50. Most of them get up to use the facilities at least twice every night, ending up with sleep problems, tiredness, irritability, and stress. The onset of nocturia is particularly distressing not only because it disrupts a good night's rest (leading to sleep-related conditions, like apnea), but also because it usually signals an underlying health problem, such as diabetes or cardiovascular diseases. Previously associated with hormonal changes, nocturia is not just a side effect of old age, but also the result of everyday lifestyle, as Tomohiro's study indicates. Professor Marcus Drake, a nocturia expert from the University of Bristol, disclosed that, until now, urologists only examined potential bladder deficiencies, prostate problems, or water intake before bedtime to account for their patients' increased urine production at night. No one thought to look into salt consumption and how it can affect nocturnal urination. With the new study emerging, Drake recognized the importance of every piece of evidence that can shed light on the matter and help medical professionals "consider all influences to get the best chance of improving the symptom." "This is an important aspect of how patients potentially can help themselves to reduce the impact of frequent urination," he said. Tomohiro's research involved 300 volunteers who unanimously reported high salt intake and sleep-related problems before the study commenced. The scientists instructed 200 of them to reduce their daily sodium consumption, from 11 grams to 8 grams (0.39 to 0.28 ounces), while 100 study participants were asked to increase their salt intake at night, from 9.6 grams to 11 grams (0.34 ounces to 0.39 ounces). Researchers monitored both groups for three months. Study results revealed the first group experienced a decrease in urinary frequency during the night, with the number of habitual visits to the bathroom dropping from 2.3 to just 1.4. Reduced salt intake also diminished their need to urinate during the day, with study participants also reporting a considerable increase in their quality of life. By comparison, people in the second group found that, after eating more salt than usual, their number of nightly trips to the toilet increased, from 2.3 to 2.7 times a night. As per the American Heart Association's guidelines, daily sodium consumption should not exceed 2.3 grams (0.08 ounces), or about a teaspoon of salt. The recommended intake of table salt, which contains around 40 percent sodium, is 1.5 grams (0.05 ounces) at the most. © 2017 Tech Times, All rights reserved. Do not reproduce without permission.
Komori T.,Nagasaki University
Cell and Tissue Research | Year: 2010
RUNX2 is a multifunctional transcription factor that controls skeletal development by regulating the differentiation of chondrocytes and osteoblasts and the expression of many extracellular matrix protein genes during chondrocyte and osteoblast differentiation. This transcription factor plays a major role at the late stage of chondrocyte differentiation: it is required for chondrocyte maturation and regulates Col10a1 expression in hypertrophic chondrocytes and the expression of Spp1, Ibsp, and Mmp13 in terminal hypertrophic chondrocytes. It is essential for the commitment of pluripotent mesenchymal cells to the osteoblast lineage. During osteoblast differentiation, RUNX2 upregulates the expression of bone matrix protein genes including Col1a1, Spp1, Ibsp, Bglap, and Fn1 in vitro and activates many promoters including those of Col1a1, Col1a2, Spp1, Bglap, and Mmp13. However, overexpression of Runx2 inhibits osteoblast maturation and reduces Col1a1 and Bglap expression. The inhibition of RUNX2 in mature osteoblasts does not reduce the expression of Col1a1 and Bglap in mice. Thus, RUNX2 directs pluripotent mesenchymal cells to the osteoblast lineage, triggers the expression of major bone matrix protein genes, and keeps the osteoblasts in an immature stage, but does not play a major role in the maintenance of the expression of Col1a1 or Bglap in mature osteoblasts. During bone development, RUNX2 induces osteoblast differentiation and increases the number of immature osteoblasts, which form immature bone, whereas Runx2 expression has to be downregulated for differentiation into mature osteoblasts, which form mature bone. During dentinogenesis, Runx2 expression is downregulated, and RUNX2 inhibits the terminal differentiation of odontoblasts. © 2009 Springer-Verlag.
Komori T.,Nagasaki University
Journal of Cellular Biochemistry | Year: 2011
RUNX2 is an essential transcription factor for osteoblast differentiation and chondrocyte maturation. SP7, another transcription factor, is required for osteoblast differentiation. Major signaling pathways, including FGF, Wnt, and IHH, also play important roles in skeletal development. RUNX2 regulates Sp7 expression at an early stage of osteoblast differentiation. FGF2 upregulates Runx2 expression and activates RUNX2, and gain-of-function mutations of FGFRs cause craniosynostosis and limb defect with upregulation of Runx2 expression. Wnt signaling upregulates Runx2 expression and activates RUNX2, and RUNX2 induces Tcf7 expression. IHH is required for Runx2 expression in osteoprogenitor cells during endochondral bone development, and RUNX2 directly regulates Ihh expression in chondrocytes. Thus, RUNX2 regulates osteoblast differentiation and chondrocyte maturation through the network with SP7 and with FGF, Wnt, and IHH signaling pathways during skeletal development. © 2010 Wiley-Liss, Inc.
Nakamura M.,Nagasaki University
Seminars in Liver Disease | Year: 2014
Antimitochondrial, anti-gp210, anti-sp100, and anticentromere antibodies are specifically detected in primary biliary cirrhosis (PBC). In clinical practice, they are useful for the diagnosis of PBC or for evaluating disease severity, clinical phenotype, and long-term outcome. In the typical or classical form of PBC which shows slow progressive loss of small bile ducts with a parallel increase in liver fibrosis, anti-gp210 antibodies are a strong risk factor for progression to jaundice and hepatic failure, whereas the presence of anticentromere antibodies is a risk factor for progression to cirrhosis and portal hypertension. Of note, the autoimmune repertoire, which is established during the early stage of the disease process, can influence the clinical phenotype and the long-term prognosis of PBC. Because the natural course of PBC is being altered by treatment with ursodeoxycholic acid, the clinical significance of these PBC-specific autoantibodies awaits re-evaluation in various ethnicities. Copyright © 2014 by Thieme Medical Publishers, Inc.
Saga University and Nagasaki University | Date: 2016-08-24
There is provided a crack detection system in which a crack can properly be detected from a strain distribution of a part to be detected, as acquired without destroying a coating layer of the part to be detected, by applying heat to the part to be detected of a detection object, and analyzing, by a digital image correlation method, images as taken before and after applying the heat to the coating layer of the part to be detected.After taking the image of the part 51 to be detected of the detection object 50 by the imaging unit 10, the heat is applied by the heating unit, and change of the part to be detected, by heat, is also caused on the other surface side through the outer coating surface of the part to be detected, which is to be moved together with the part to be detected. Accordingly, images of every portions of the coating surface of the part to be detected are taken and the image analysis unit 30 analyzes the images before and after applying the heat to acquire a strain distribution of the part to be detected, so that the crack can be detected based on difference in a state of strain between a place where the crack exist and the other place.Therefore, taking the images of the part to be detected including its coating layer enables the analysis to progress without any problems to detect the crack, without removing the coating layer, thus improving the work efficiency of the detection operation.
Nagasaki University, Usaien Pharmaceutical Co. and Amino Up Chemical Co. | Date: 2015-12-21
The present invention relates to a composition containing as its main component proanthocyanidin oligomer to which a substance having a phloroglucinol ring structure or resorcinol ring structure has been bonded and reduced in the molecular weight, which is obtained by heating plant materials containing proanthocyanidin polymer or extract thereof with a substance having a phloroglucinol ring structure or resorcinol ring structure in an acidic aqueous solution, production method thereof, and uses of the composition in health products and pharmaceutical products. According to the invention, proanthocyanidin oligomer having physiological activity, to which a substance having a phloroglucinol ring structure or resorcinol ring structure has been bonded and reduced in the molecular weight to such a level that the oligomer can be absorbed into living body, which has been conventionally difficult to obtain at high yield from plant raw materials, can be produced efficiently and easily.
Nagasaki University and Panasonic | Date: 2015-04-08
The control device 1A includes an on-time information generation circuit 11, a zero cross detecting circuit 12 and a PWM signal generation circuit 13. The on-time information generation circuit 11 inputs at least a power converter circuit information including an output voltage value of a power converter circuit 2, and generates the on-time information about a switch 212. The zero cross detecting circuit 12 detects a time when a inductor current becomes zero by inputtin a voltage between both terminals of the inductor 214, and generates a zero cross detection signal when the inductor current became zero. The PWM signal generation circuit 13 inputs the on-time information and the zero cross detection signal, and generates a turn on signal and a turnoff signal. The zero cross detecting circuit 12 has an edge detecting circuit. The zero cross detecting circuit 12 generates a zero cross detection signal when the edge detecting circuit detected an edge appearing in a voltage between both terminals of the inductor 214. The PWM signal generation circuit 13 generates a turn-on signal when a zero cross detection signal was input. The PWM signal generation circuit 13 generates the turn-off signal, when a time based on the on-time information passed, In this way, by the present invention, a change of the inductor current is acquired precisely, and a good critical mode control is carried out.
Nagasaki University | Date: 2015-03-30
The present invention aims to provide a novel compound for measuring cellular cytotoxicity or cell proliferation capacity accurately with high reproducibility, conveniently and rapidly, and a measurement method of cellular cytotoxicity or cell proliferation capacity by using the compound. The present invention relates to a compound represented by the formula (I): wherein R^(1 )is a substituent, R^(2 )and R^(3 )are each an optionally substituted hydrocarbon group, or an optionally substituted heterocyclic group, Y is a substituent, n is an integer of 0-3, Z is a single bond, O, S, SO, SO_(2), or NR^(4) (R^(4 )is a hydrogen atom or a substituent), and A is an optionally substituted C_(1-6 )alkylene group) or a salt thereof.