Shiga University of Medical Science

www.shiga-med.ac.jp
Otsu-shi, Japan

Shiga University of Medical Science is a national university in Ōtsu, Shiga, Japan, founded in 1974. Wikipedia.

SEARCH FILTERS
Time filter
Source Type

Patent
Tocalo Co. and Shiga University of Medical Science | Date: 2017-08-09

There is provided an energy device for surgical operation capable of suppressing fixation of body tissue, wherein a coating layer (14) is formed on an outer periphery of a base material (11) constituting an operational area portion transmitting energy in an energy device for surgical operation operating in the operational area portion, and is comprised of a base coating (12) formed on the base material and an outermost coating (13) formed on the base coating. The base coating is made from silicon oxide or a compound containing silicon oxide, and the outermost coating is made from polysiloxane or a compound containing polysiloxane or a compound containing a partly fluorinated polysiloxane, and the coating layer has a good adhesiveness and is applicable to a complicated form.


Patent
Shiga University of Medical Science | Date: 2015-03-17

The inventions disclosed herein are a method for quantifying cardiolipin in a sample, comprising the steps of: (1) treating the sample with phospholipase D, glycerol kinase, glycerol-3-phosphate oxidase, and peroxidase and (2) measuring the fluorescence intensity, absorbance, or luminescence intensity of a compound generated in step (1) to quantify cardiolipin using a calibration curve obtained beforehand; and a kit for quantifying cardiolipin comprising phospholipase D, glycerol kinase, glycerol-3-phosphate oxidase, and peroxidase.


Morita S.-Y.,Shiga University of Medical Science
Biological and Pharmaceutical Bulletin | Year: 2016

Increased levels of apolipoprotein B (apoB)-containing lipoproteins, such as low density lipoproteins (LDL) and chylomicron remnants, are associated with the development of atherosclerosis. Chylomicrons containing apoB-48 are secreted from the intestine during the postprandial state, whereas very low density lipoproteins (VLDL) containing apoB-100 are constitutively formed in the liver. Chylomicron remnants and VLDL remnants are produced by the lipoprotein lipase-mediated lipolysis of triglycerides, which is activated by apolipoprotein C-II bound on the particle surfaces. The hepatic uptake of these remnants is facilitated by apolipoprotein E (apoE), but is inhibited by apolipoproteins C-I, C-II and C-III. In the plasma, VLDL remnants are further converted into LDL by the hydrolysis of triglycerides. ApoB-100 is responsible for the hepatic uptake of LDL. LDL receptor, LDL receptor-related protein and heparan sulfate proteoglycans are involved in the hepatic clearance of lipoproteins containing apoB-100 and/or apoE. The subendothelial retention and modification of apoB-containing lipoproteins are crucial events in the initiation of atherosclerosis. In the subendothelium, the uptake of modified lipoproteins by macrophages leads to the formation of foam cells storing excess amounts of cholesteryl esters and subsequently to apoptosis. This review describes the current knowledge about the metabolism and modification of apoB-containing lipoproteins involved in dyslipidemia and atherogenesis. In particular, I focus on the effects of apolipoproteins, lipid composition and particle size on lipoprotein metabolism and on the roles of cholesterol, sphingomyelinase and apoB denaturation in macrophage foam cell formation and apoptosis. A detailed understanding of these mechanisms will help to develop new therapeutic strategies. © 2016 The Pharmaceutical Society of Japan.


Takano T.,Shiga University of Medical Science
Developmental Neuroscience | Year: 2015

Autism is an extremely heterogeneous disorder, but its frequent cooccurrence with epilepsy leads to speculation that there may be common mechanisms associated with these disorders. Inhibitory interneurons are considered to be the main cellular elements that control hyperexcitability in the brain, and interneuron dysfunction can cause pathological hyperexcitability linked to seizure susceptibility or epilepsy. This review summarizes some of the recent advances that support the relationship between interneuron dysfunction and cognitive impairment in human syndromic autism, with particular reference to the pathophysiological findings of murine experimental models of autism. Alterations in γ-aminobutyric acid (GABA)ergic circuits include a wide variety of neurobiological dysfunctions and do not simply involve the loss or gain of any given type of inhibitory mechanism. The characteristics of interneuron dysfunction in each murine model of autism differ for each syndrome, and these diversities may be due to differences in genetic backgrounds or some other currently unknown variances. Future studies should give us a greater understanding of the involvement of different classes of GABAergic interneurons and allow us to define the relationship between the precise pathophysiological mechanisms and the corresponding clinical phenotypes in autism. © 2015 S. Karger AG, Basel.


Patent
Ehime University, Shiga University of Medical Science and Yokohama City University | Date: 2015-11-04

Provided in the present invention is a genetic marker including a SNP which can be used for assessing the risk of developing hypertension, a polynucleotide for assessing the risk of developing hypertension which can be used as a primer or probe for detecting the genetic marker, a method for assessing the risk of developing hypertension using the SNP, a microarray for assessing the risk of developing hypertension which is used for genotyping of the SNP, a kit used in the method for assessing the risk of developing hypertension, and the like.


Patent
Ehime University, Shiga University of Medical Science and Yokohama City University | Date: 2015-10-28

Provided in the present invention is a genetic marker including a SNP which can be used for assessing the risk of developing hypertension, a polynucleotide for assessing the risk of developing hypertension which can be used as a primer or probe for detecting the genetic marker, a method for assessing the risk of developing hypertension using the SNP, a microarray for assessing the risk of developing hypertension which is used for genotyping of the SNP, a kit used in the method for assessing the risk of developing hypertension, and the like.


Modification of serine and threonine residues in proteins by O-linked β-N-acetylgulcosamine (O-GlcNAc) glycosylation is a feature of many cellular responses to the nutritional state and to stress. O-GlcNAc modification is reversibly regulated by O-linked β-N-acetylgulcosamine transferase (OGT) and β-D-N-acetylgulcosaminase (O-GlcNAcase). O-GlcNAc modification of proteins is dependent on the concentration of uridine 5′-diphospho-N-acetylgulcosamine (UDP-GlcNAc), which is a substrate of OGT and is synthesized via the hexosamine biosynthetic pathway. Immunoblot analysis using the O-GlcNAc-specific antibody CTD110.6 has indicated that glucose deprivation increases protein O-GlcNAcylation in some cancer cells. The mechanism of this paradoxical phenomenon has remained unclear. Here we show that the increased glycosylation induced by glucose deprivation and detected by CTD110.6 antibodies is actually modification by N-GlcNAc2, rather than by O-GlcNAc. We found that this induced glycosylation was not regulated by OGT and O-GlcNAcase, unlike typical O-GlcNAcylation, and it was inhibited by treatment with tunicamycin, an N-glycosylation inhibitor. Proteomics analysis showed that proteins modified by this induced glycosylation were N-GlcNAc2-modified glycoproteins. Furthermore, CTD110.6 antibodies reacted with N-GlcNAc2-modified glycoproteins produced by a yeast strain with a ts-mutant of ALG1 that could not add a mannose residue to dolichol-PP-GlcNAc2. Our results demonstrated that N-GlcNAc2-modified glycoproteins were induced under glucose deprivation and that they cross-reacted with the O-GlcNAc-specific antibody CTD110.6. We therefore propose that the glycosylation status of proteins previously classified as O-GlcNAc-modified proteins according to their reactivity with CTD110.6 antibodies must be re-examined. We also suggest that the repression of mature N-linked glycoproteins due to increased levels of N-GlcNAc2-modifed proteins is a newly recognized pathway for effective use of sugar under stress and deprivation conditions. Further research is needed to clarify the physiological and pathological roles of N-GlcNAc2-modifed proteins. © 2011 Takahiro Isono.


Patent
Shiga University of Medical Science | Date: 2015-11-18

Disclosed is a compound represented by formula (1) or a salt thereof, formula (1) :^(1) and R^(2) are each independently a hydrogen atom, a fluorine atom, methyl, or trifluoromethyl; R^(3) is trifluoromethyl or trifluoromethoxy; and p is an integer of 1 to 4, provided that m + n 5 when J is J-1, and m + n 7 when J is J-2 or J-3.


Patent
Shiga University of Medical Science | Date: 2015-03-25

It is an object to provide a surgical tool for excising a hard solid organ such as cirrhotic liver or cutting the organ into a groove without causing bleeding. The inventors of the present invention have found that an organ resection tool including a brush-like structure capable of performing microwave irradiation and/or a brush-like structure capable of receiving a microwave can achieve the above-mentioned object, to thereby arrive at the present invention (organ resection tool including a brush structure capable of performing microwave irradiation). For example, an organ can be crushed or scraped away by manually abrading the organ with a brush of a solid organ resection tool including a brush structure capable of performing microwave irradiation according to the present invention. Further, the organ can be concurrently coagulated through the microwave irradiation to stop bleeding.


Patent
Shiga University of Medical Science | Date: 2014-10-22

Provided is a surgical instrument that is substitutable for an operation of placing each stitch with a threaded needle or a stapler. It is confirmed that, in a tissue suturing device including a crushing section, and a projecting section including a central conductor and/or an external conductor for applying a microwave, the projecting section and the crushing section bring fragmentary portions of tissues to be sutured into contact or overlap with each other, and coagulate and/or fix contact or overlap portions with the microwave, to thereby stitch the tissues to be sutured.

Loading Shiga University of Medical Science collaborators
Loading Shiga University of Medical Science collaborators