News Article | May 22, 2017
Liver cirrhosis is the 12th leading cause of mortality worldwide and approximately half of those deaths are due to alcohol abuse. Yet apart from alcohol abstinence, there are no specific treatments to reduce the severity of alcohol-associated liver disease. Researchers at University of California San Diego School of Medicine and J. Craig Venter Institute (JCVI) have linked intestinal fungi to increased risk of death for patients with alcohol-related liver disease. They also found that antifungal treatment protects mice from alcohol-related liver disease progression. The study is published May 22 in the Journal of Clinical Investigation. "Not only is this the first study to associate fungi and liver disease," said senior author Bernd Schnabl, MD, associate professor of gastroenterology at UC San Diego School of Medicine, "we might be able to to slow the progression of alcoholic liver disease by manipulating the balance of fungal species living in a patient's intestine." Alcoholism is associated with bacterial overgrowth in the intestines, as well as a shift in the types of bacteria found there, but little was known about the role of intestinal fungi in alcoholic liver disease. In this study, Schnabl and colleagues found that fungi flourished in the intestines of mice with chronic alcohol exposure. In turn, they noted, the fungal overgrowth exacerbated liver disease. Parts of the fungal cell wall, mainly a sugar called beta-glucan, moved through the mouse's intestinal wall into the surrounding body cavity and organs. Once relocated inside the liver, beta-glucan bound certain immune cells and triggered inflammation. Chronic inflammation kills liver cells and ultimately promotes alcoholic liver disease. But the researchers were able to protect mice from alcohol-induced liver disease by treating them with the antifungal compound amphotericin B. Compared to untreated mice, mice with alcohol-related liver disease that received amphotericin B had lower levels of liver injury and fat accumulation. These outcomes were determined by measuring plasma levels of a liver enzyme called alanine aminotransferase (reduced by approximately 55 percent) and levels of liver triglycerides (reduced by approximately 21 percent). In this study, the mice received a type of oral amphotericin B that is not absorbed into the bloodstream. The drug only acts locally in the intestine and thus did not cause systemic side effects. Because it has no effect on systemic fungal infections, oral amphotericin B is not FDA-approved for human use. Intravenous amphotericin B is FDA approved for the treatment of serious fungal infections and it can cause side effects such as stomach, bone, muscle or joint pain and shortness of breath. "This work demonstrates that alcoholic liver disease is exacerbated not only by bacteria, but also by fungi. Therefore, therapeutic strategies that target both need to be translated into clinical practice," said co-author Derrick Fouts, PhD, professor of genomic medicine at JCVI. "This study suggests a greater role of fungi in modulating the human microbiome than previously appreciated." The team also compared fungi in the stool of eight healthy people and 20 people with chronic alcohol abuse and various stages of liver disease. They found that the healthy people had a richer diversity of fungi living in their intestines, as compared to alcohol-dependent patients. Instead, alcohol-dependent patients at all stages of liver disease had dramatic overgrowths of one fungal type in particular -- Candida, which includes the species that causes yeast infections. In addition, Schnabl's team found a correlation between fungi and disease severity in a separate group of 27 patients with alcohol-related liver disease: The higher the exposure to fungi, as measured by a person's level of antibodies that recognize them, the higher the risk of death. Fourteen patients had high fungi levels and 13 were classified as low. After five years, 77 percent of the low-fungi group survived, compared to 36 percent of the high-fungi group. Schnabl cautioned that this human study is just proof-of-concept in a relatively small number of patients. In addition, he said it might not be the changes in fungal populations that cause progression of alcoholic liver disease. Rather, it could be the overgrowth of intestinal fungi in combination with leaky intestinal walls -- a known result of alcohol abuse -- that trigger chronic inflammatory responses in the liver. Further studies are needed to determine if a single fungal species contributes to liver disease progression more than others. "Since it was so effective in mice, we are interested in testing amphotericin B in patients with alcohol-related liver disease -- a population in urgent need of new therapeutics," Schnabl said. Co-authors of this study include: An-Ming Yang, UC San Diego and En Chu Kong Hospital, Taiwan; Tatsuo Inamine, UC San Diego and Nagasaki University; Katrin Hochrath, Peng Chen, Sena Bluemel, Phillipp Hartmann, Jun Xu, Yukinori Koyama, Tatiana Kisseleva, Hal M. Hoffman, UC San Diego; Lirui Wang, Cristina Llorente, Samuel B. Ho, UC San Diego and VA San Diego Healthcare System; Manolito G. Torralba, Kelvin Moncera, Karen Beeri, J. Craig Venter Institute; Chien-Sheng Chen, National Central University, Taiwan; Kim Freese, Claus Hellerbrand, Friedrich-Alexander University Erlangen- Nürnberg; Serene M.L. Lee, Hospital of the LMU Munich; Wajahat Z. Mehal, Guadalupe Garcia-Tsao, Yale University and VA-CT Healthcare System; Ece A. Mutlu, Ali Keshavarzian, Rush University Medical Center; Gordon D. Brown, University of Aberdeen; Ramon Bataller, University of North Carolina at Chapel Hill; and Peter Stärkel, St. Luc University Hospital, Université Catholique de Louvain, Brussels.
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.
Nagasaki University and Figaro Engineering Inc. | Date: 2016-02-05
A CO sensor includes a solid electrolyte substrate, a sensing electrode, and a reference electrode, and outputs electromotive forces in accordance with CO concentrations. The sensing electrode and the reference electrode are provided on the same surface of the solid electrolyte substrate. The sensing electrode contains a metal oxide such as Bi_(2)O_(3 )that generates a positive electromotive force response when coming into contact with CO. The reference electrode contains a metal oxide such as CeO_(2 )that generates a negative electromotive force response when coming into contact with CO.
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.
Nagasaki University | Date: 2015-03-26
[Problem] To reduce the risk of damaging organs in a body while delivering a thread during surgery. [Means for Solving Problem] An instrument for delivering a surgical thread has a grip 10, an outer cylinder 70 fixed the grip, a hollow needle 80 extending inside the outer cylinder 70 and being configured to be moved relative to the outer cylinder 70 in an axial direction and a loop 90 configured to be housed in the outer cylinder 70. An end of the outer cylinder 70 is bent in a state where force is not applied. The hollow needle 80 is exposed from the outer cylinder 70 when puncturing skin or etc., and the hollow needle 80 is housed in the outer cylinder 70 when it travels near organs which should not be damaged.
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.