Kyoto, Japan

Kyoto Prefectural University of Medicine is a public university in Kyoto, Kyoto, Japan. The predecessor of the school was founded in 1872, and it was chartered as a university in 1921. Wikipedia.


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News Article | May 18, 2017
Site: www.eurekalert.org

Opitz G/BBB (Opitz) syndrome is a hereditary disorder that affects people in different ways, causing malformations in medial (midline) organs and structures, intellectual disability and developmental disorders. Scientists have revealed a new control mechanism for the gene that causes this disorder, a discovery that could help in developing treatment for the syndrome. The findings were published on May 16 in the online edition of Development. A group of scientists led by Associate Professor UEYAMA Takehiko and Professor SAITO Naoaki (both from the Kobe University Biosignal Research Center) and members of Kyoto Prefectural University of Medicine carried out this research. Professor Ueyama expressed his hopes that this discovery would contribute to "revealing the underlying mechanism that explains the range of symptoms caused by Opitz syndrome, a disease that has different effects on individual patients, even within the same family". Opitz syndrome occurs for at least 1 in every 10,000-50,000 people. It is a hereditary disorder that causes a wide range of physical malformations in midline structures of organs, including in the brain, the face, the heart, the larynx and pharynx, the trachea and esophagus, urinary organs and genitals. Previous findings identified Midline 1 (MID1) as the gene responsible for Opitz syndrome. The functional decline of MID1 causes the congenital disorders described above, but it is still unclear why these symptoms are so varied among individual patients. Treatment methods are yet to be fixed, and surgical therapy is currently the main treatment. The research team focused on cerebellar granule neurons, a type of neurons with the largest population in the brain, and a signaling protein/molecule called Rac which functions in cerebellar granule neurons during cerebellar development. The team created a "knockout" mouse with the Rac protein deleted. They discovered that this mouse experienced severe walking impairment because of the loss of the internal granule layer in the medial cerebellum. Next, they extracted the cerebellar granule neurons affected by the deleted Rac from the medial cerebellum. Using DNA microarrays they examined these neurons and discovered reduced expression of MID1, the causative gene of Opitz syndrome. This showed that Rac had been regulating the expression of Mid1, and when Rac was deleted, MID1 stopped functioning correctly in the mouse. They also discovered a cell signaling pathway in which Rac-Mid1-mTOR form a complex and contribute to the differentiation and maturation of cerebellar granule cells. The individual variability in these cell signaling pathways could be a cause of the broad range in the symptoms caused by Opitz syndrome. These findings could lead to development of a new treatment for Opitz syndrome that targets cell signaling.


News Article | May 19, 2017
Site: www.sciencedaily.com

Opitz G/BBB (Opitz) syndrome is a hereditary disorder that affects people in different ways, causing malformations in medial (midline) organs and structures, intellectual disability and developmental disorders. Scientists have revealed a new control mechanism for the gene that causes this disorder, a discovery that could help in developing treatment for the syndrome. The findings were published on May 16 in the online edition of Development. A group of scientists led by Associate Professor UEYAMA Takehiko and Professor SAITO Naoaki (both from the Kobe University Biosignal Research Center) and members of Kyoto Prefectural University of Medicine carried out this research. Professor Ueyama expressed his hopes that this discovery would contribute to "revealing the underlying mechanism that explains the range of symptoms caused by Opitz syndrome, a disease that has different effects on individual patients, even within the same family." Opitz syndrome occurs for at least 1 in every 10,000-50,000 people. It is a hereditary disorder that causes a wide range of physical malformations in midline structures of organs, including in the brain, the face, the heart, the larynx and pharynx, the trachea and esophagus, urinary organs and genitals. Previous findings identified Midline 1 (MID1) as the gene responsible for Opitz syndrome. The functional decline of MID1 causes the congenital disorders described above, but it is still unclear why these symptoms are so varied among individual patients. Treatment methods are yet to be fixed, and surgical therapy is currently the main treatment. The research team focused on cerebellar granule neurons, a type of neurons with the largest population in the brain, and a signaling protein/molecule called Rac which functions in cerebellar granule neurons during cerebellar development. The team created a "knockout" mouse with the Rac protein deleted. They discovered that this mouse experienced severe walking impairment because of the loss of the internal granule layer in the medial cerebellum. Next, they extracted the cerebellar granule neurons affected by the deleted Rac from the medial cerebellum. Using DNA microarrays they examined these neurons and discovered reduced expression of MID1, the causative gene of Opitz syndrome. This showed that Rac had been regulating the expression of Mid1, and when Rac was deleted, MID1 stopped functioning correctly in the mouse. They also discovered a cell signaling pathway in which Rac-Mid1-mTOR form a complex and contribute to the differentiation and maturation of cerebellar granule cells. The individual variability in these cell signaling pathways could be a cause of the broad range in the symptoms caused by Opitz syndrome. These findings could lead to development of a new treatment for Opitz syndrome that targets cell signaling.


Ryang S.,Kyoto Prefectural University of Medicine
Physics Letters, Section B: Nuclear, Elementary Particle and High-Energy Physics | Year: 2012

We consider an extremal three-point correlator of three heavy vertex operators for the circular winding string state with one large spin and one winding number in AdS 5 and one large spin and one winding number in S 5. We use a Schwarz-Christoffel transformation to compute semiclassically the extremal three-point correlator on a stationary string trajectory which is mapped to the complex plane with three punctures. It becomes a 4d conformal invariant three-point correlator on the boundary. We discuss the marginality condition of vertex operator. © 2012.


Ryang S.,Kyoto Prefectural University of Medicine
Journal of High Energy Physics | Year: 2011

We compute semiclassically the two-point correlator of the marginal vertex operators describing the rigid circular spinning string state with one large spin and one windining number in AdS5 and three large spins and three winding numbers in S5. The marginality condition and the conformal invariant expression for the two-point correlator obtained by using an appropriate vertex operator are shown to be associated with the diagonal and off-diagonal Virasoro constraints respectively. We evaluate semiclassically the three-point correlator of two heavy circular string vertex operators and one zero-momentum dilaton vertex operator and discuss its relation with the derivative of the dimension of the heavy circular string state with respect to the string tension. © SISSA 2011.


Ishii S.,Kyoto Prefectural University of Medicine
Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies | Year: 2013

To determine whether ultrasound guidance increases the success rates, decreases the complication rates, and shortens the time to successful radial artery catheterization in infants and small children. Randomized study. Single university-affiliated hospital. Infants and children weighing 3-20 kg, undergoing cardiac surgery for congenital heart disease. We randomly assigned the right and left radial arteries of patients undergoing arterial catheterization to ultrasound-guided technique versus the usual palpation technique. The primary study endpoints were the rates of successful cannulation at first and within three attempts. The secondary endpoints were time to radial artery identification, number of attempts for successful cannulation, and rate of complications. Compared with palpation, ultrasound-guided radial artery catheterization was successful in 76.3% versus 35.6% of first attempts and in 94.9% versus 50.8% of arteries after three attempts (both comparisons, p < 0.01). The median time [interquartile range] to identification of the arteries (18.5 seconds [11.25-27.25] vs 30 seconds [17.75-39.5]) was significantly shorter (p < 0.01), the number of attempts [interquartile range] at successful cannulation (1 [1-1] vs 2 [1-2]) was significantly fewer (p < 0.01), and the proportion of hematomas (5.1% vs 25.4%) was significantly lower (p < 0.01) in the ultrasound group than those in the palpation group. In infants and small children, ultrasound-guided radial artery catheterization was more successful and expeditious than the usual palpation technique.


Fushiki S.,Kyoto Prefectural University of Medicine
Brain and Development | Year: 2013

On March 11, 2011, Japan was hit by the Great East Japan Earthquake followed by the Fukushima Daiichi Nuclear Disaster. Firstly, this review focuses on what happened after the accidents at the Three Mile Island nuclear power station in 1979 and the Chernobyl nuclear power plant in 1986, in terms of the effects of these incidents on health. The most critical issue when considering the effects of radiation on the health of children was the increase of thyroid cancer, as clearly demonstrated among people who were children or adolescence at the time of the Chernobyl accident. Therefore, in the early days after a nuclear accident, the primary concern should be efforts to prevent the exposure of children to radioactive iodine through inhalation and ingestion, because radioactive iodine preferentially accumulates in the thyroid. In the longer term, another concern is exposure to radionuclides with long half-lives, including cesium137 and cesium134, with physical half-lives of 30 and 2. years, respectively. Secondly, fetal radiation risks and radiobiological studies on low-level radiation are briefly reviewed, with reference to the effects upon the developing brain. A fetal dose of 100. mSv may increase the risk of an effect on brain development, especially neuronal migration, based upon the results of experiments with rodents. Finally, this review proposes that research on the health effects of low level radiation should be prioritized so that accurate information on the effects of radiation can be disseminated and prevent the prevalence of unnecessary fear lacking scientific justification. © 2012 The Japanese Society of Child Neurology.


Maruyama K.,Kyoto Prefectural University of Medicine
Investigative ophthalmology & visual science | Year: 2012

It has been shown previously that the presence in the cornea of antigen-presenting cells (APC), such as macrophages (MPS) and lymphangiogenesis, is a risk for corneal transplantation. We sought to determine whether the existence of lymphatic vessels in the non-inflamed cornea is associated with the presence of MPS. Flat mounts were prepared from corneas of untreated C57BL/6, CD11b(-/-), F4/80(-/-), and BALB/c mice, and after suture placement or corneal transplantation, observed by immunofluorescence for the presence of lymphatic vessels using LYVE-1 as a marker of lymphatic endothelium. Innate immune cells were detected in normal mouse corneas using CD11b, F4/80, CD40, as well as MHC-class II. Digital images of the flat mounts were taken using a spot image analysis system, and the area covered by lymphatic vessels was measured using NIH Image software. The number of spontaneous lymphatic vessels in C57BL/6 corneas was significantly greater than in BALB/c corneas (P = 0.03). There were more CD11b(+) (P < 0.01) and CD40(+), MHC-class II (+) cells in the C57BL/6 corneas than in BALB/c mouse corneas. MPS depletion via clodronate liposome in C57BL/6 mice led to fewer spontaneous lymphatic vessels and reduced inflammation-induced lymphangiogenesis relative to control mice. Mice deficient in CD11b or F4/80 had fewer spontaneous lymphatic vessels and less lymphangiogenesis than control C57BL/6 mice. C57BL/6 mouse corneas have more endogenous CD11b(+) cells and lymphatic vessels. The endogenous lymphatic vessels, along with pro-inflammatory MPS, account for the high risk of corneal graft rejection in C57BL/6 mice. CD11b(+) and F4/80(+) MPS appear to have an important role in of the formation of new lymphatic vessels.


Kitaya K.,Kyoto Prefectural University of Medicine
Fertility and Sterility | Year: 2011

Chronic endometritis was identified immunohistochemically in 9.3% of patients with recurrent miscarriages (in 12.9% of patients with miscarriages of unknown etiology). Chronic endometritis is not negligible in patients with recurrent miscarriages. ©2011 by American Society for Reproductive Medicine.


Akakabe Y.,Kyoto Prefectural University of Medicine
Nature communications | Year: 2013

Insulin resistance is closely associated with obesity and is one of the earliest symptoms of type-2 diabetes. Endothelial cells are involved in the pathogenesis of insulin resistance through their role in insulin delivery and adipose tissue angiogenesis. Here we show that Ecscr (endothelial cell surface expressed chemotaxis and apoptosis regulator; also known as ARIA), the transmembrane protein that regulates endothelial cell signalling, is highly expressed in white and brown adipose tissues, and regulates energy metabolism and glucose homeostasis by modulating endothelial cell functions. Ecscr-deficient mice fed a normal chow show improved glucose tolerance and enhanced insulin sensitivity. We demonstrate that Ecscr deletion enhances the insulin-mediated Akt/endothelial nitric oxide synthase activation in endothelial cells, which increases insulin delivery into the skeletal muscle. Ecscr deletion also protects mice on a high-fat diet from obesity and obesity-related metabolic disorders by enhancing adipose tissue angiogenesis. Conversely, targeted activation of Ecscr in endothelial cells impairs glucose tolerance and predisposes mice to diet-induced obesity. Our results suggest that the inactivation of Ecscr enhances insulin sensitivity and may represent a new therapeutic strategy for treating metabolic syndrome.


Nomura T.,Kyoto Prefectural University of Medicine
Nature communications | Year: 2013

The emergence of larger brains with large numbers of neurons is an evolutionary innovation in mammals and birds. However, the corresponding changes in cortical developmental programmes during amniote evolution are poorly understood. Here we examine the cortical development of Madagascar ground geckos, and report unique characteristics of their reptilian cortical progenitors. The rates of proliferation and neuronal differentiation in the gecko cortex are much lower than those in other amniotes. Notch signalling is highly activated in the gecko cortical progenitors, which provides a molecular basis for the low rate of cortical neurogenesis. Interestingly, multiple neuron subtypes are sequentially generated in the gecko cortex, similar to other amniotes. These results suggest that changes in the regulation of cortical neural progenitors have accelerated neurogenesis and provided encephalization in mammalian and archosaurian lineages. In addition, the temporal regulation for making cortical neuronal subtypes has evolved in a common ancestor(s) of amniotes.

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