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Institution

Hyogo College of Medicine

EducationNishinomiya, Hyôgo, Japan
About: Hyogo College of Medicine is a education organization based out in Nishinomiya, Hyôgo, Japan. It is known for research contribution in the topics: Cancer & Transplantation. The organization has 5030 authors who have published 10629 publications receiving 258734 citations. The organization is also known as: Hyōgo ika daigaku.


Papers
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Journal ArticleDOI
TL;DR: A retrospective review of 122 patients with ISSD who were treated at the Department of Otolaryngology, Eye, Ear, Nose and Throat Hospital at Shanghai Medical University over a 25-year period finds the most common initial symptom was headache, followed in decreasing order by visual changes, cranial nerve palsies, and nasal symptoms.
Abstract: Solitary or isolated involvement of the sphenoid sinus (Isolated sphenoid sinus disease; ISSD ) is a relatively uncommon disease. The present study reviews retrospectively 125 patients with ISSD treated at the Departments of Otolaryngology, Eye Ear Nose and Throat Hospital, Shanghai Medical University (109), and Hyogo College of Medicine (16) over a period of 25 years. Diagnosis was made on the basis of history, signs, nasal endoscopy, imaging techniques with CT/MRI. The final diagnosis of ISSD was established after histopathological and microbiological examinations of the excisional specimen. The pathology was sphenoid sinusitis (40), sphenoid cysts (35), fungal diseases (19), malignant tumors (9), and others (20). The most common initial symptom was headache, followed by visual changes and cranial nerve palsies due to the nearby involvements. Increasing use of routine imaging techniques with CT/MRI and diagnostic nasal endoscopy resulted in the increased numbers of early ISSD. Recent nasal endoscopic ostial sphenoidotomy warrants for the precise pathological diagnosis, and at the same time for the safe and immediate treatment, prior to the sequential extension to adjacent vital structures even to the serious or fatal stage.

64 citations

Journal ArticleDOI
TL;DR: The elevation of thiOCyanate in patients undergoing dialysis probably is secondary to both limited efficiency of HD and deranged metabolism of cyanide and thiocyanate, which may play a role in uraemic complications including cardiovascular events.
Abstract: Background. Cyanide is a toxic agent, and its detoxification product, thiocyanate, may be a major pathogenetic substance in uraemia. Recent studies examining the myeloperoxidase(MPO)/thiocyanate system have suggested a link between thiocyanate and atherosclerosis. However, inaccuracies in conventional assays for cyanide and thiocyanate have limited the understanding of their metabolism in haemodialysis (HD) patients. Methods. We used high-performance liquid chromatography to measure cyanide in erythrocytes and thiocyanate in plasma in 43 HD patients and in a group of 46 healthy controls that included 15 current smokers. To clarify the metabolic conversion of cyanide to thiocyanate in uraemic patients, we also measured cysteine and sulfate. We then used stepwise regression analysis to analyse factors that determine erythrocyte cyanide and plasma thiocyanate. Results. Mean cyanide and thiocyanate were significantly greater in HD patients than in non-smoking controls. However, cyanide was far below lethal concentrations in dialysis patients. Thiocyanate was six to seven times greater in HD patients than in non-smoking controls, and decreases in thiocyanate following dialysis were only 19.3±3.5%. Multiple regression analysis showed a positive correlation between cyanide and thiocyanate in controls, but a negative correlation in HD patients. In patients, an inverse relationship between thiocyanate and BUN was also observed. Conclusions. The elevation of thiocyanate in patients undergoing dialysis probably is secondary to both limited efficiency of HD and deranged metabolism of cyanide and thiocyanate. Because thiocyanate is a preferred substrate for MPO, it may play a role in uraemic complications including cardiovascular events.

64 citations

Journal ArticleDOI
TL;DR: It is shown that non‐neuronal glial cells in the preBötC are periodically activated preceding inspiratory neuronal activity, and the previous report that blockade of astrocytic metabolism abolishes inspiratory neural output suggest thatAstrocytes are functionally involved in respiratory rhythm generation.
Abstract: otC), is the kernel for respiratory rhythm generation. Despite previous extensive studies focusing on neurons,themechanismofhowrespiratoryrhythmisgeneratedhasnotbeenfullyunderstood. • Here we show that non-neuronal glial cells (a subset of putative astrocytes) in the preB¨ are periodically activated preceding inspiratory neuronal activity, periodic activity of putative astrocytes persists during blockade of neuronal activity, and stimulation of astrocytes in the preB¨ otC induces inspiratory neuronal firings. • These findings together with the previous report that blockade of astrocytic metabolism abolishes inspiratory neural output suggest that astrocytes are functionally involved in respiratory rhythm generation. • These results will help us better understand how respiratory rhythm is generated and how respiratory output is disturbed in various pathological conditions.

64 citations

Journal ArticleDOI
TL;DR: XN treatment effectively prevented the BIG3-PHB2 interaction, thereby releasing PHB2 to directly bind to both nuclear- and cytoplasmic ERα, leading to the complete suppression of the E2-signalling pathways and ERα-positive breast cancer cell growth both in vitro and in vivo.
Abstract: Xanthohumol (XN) is a natural anticancer compound that inhibits the proliferation of oestrogen receptor-α (ERα)-positive breast cancer cells. However, the precise mechanism of the antitumour effects of XN on oestrogen (E2)-dependent cell growth, and especially its direct target molecule(s), remain(s) largely unknown. Here, we focus on whether XN directly binds to the tumour suppressor protein prohibitin 2 (PHB2), forming a novel natural antitumour compound targeting the BIG3-PHB2 complex and acting as a pivotal modulator of E2/ERα signalling in breast cancer cells. XN treatment effectively prevented the BIG3-PHB2 interaction, thereby releasing PHB2 to directly bind to both nuclear- and cytoplasmic ERα. This event led to the complete suppression of the E2-signalling pathways and ERα-positive breast cancer cell growth both in vitro and in vivo, but did not suppress the growth of normal mammary epithelial cells. Our findings suggest that XN may be a promising natural compound to suppress the growth of luminal-type breast cancer.

64 citations

Journal ArticleDOI
TL;DR: It is suggested that hypermethylation of CDH13 is a common, tissue‐specific event in human EAC, occurs early during BE‐associated neoplastic progression, and correlates with known clinical neoplastics progression risk factors.
Abstract: Although the CDH13 gene has been shown to undergo epigenetic silencing by promoter methylation in many types of tumors, hypermethylation of this gene in Barrett's-associated esophageal adenocarcinogenesis has not been studied. Two hundred fifty-nine human esophageal tissues were therefore examined for CDH13 promoter hypermethylation by real-time methylation-specific PCR. CDH13 hypermethylation showed discriminative receiver-operator characteristic curve profiles, sharply demarcating esophageal adenocarcinoma (EAC) from esophageal squamous cell carcinoma (ESCC) and normal esophagus (NE) (p < 0.0001). CDH13 normalized methylation values (NMV) were significantly higher in Barrett's esophagus (BE), dysplastic BE (D) and EAC than in NE (p < 0.0000001). CDH13 hypermethylation frequency was 0% in NE but increased early during neoplastic progression, rising to 70% in BE, 77.5% in D and 76.1% in EAC. Both CDH13 hypermethylation frequency and its mean NMV were significantly higher in BE with than without accompanying EAC. In contrast, only 5 (19.2%) of 26 ESCCs exhibited CDH13 hypermethylation. Furthermore, both CDH13 hypermethylation frequency and its mean NMV were significantly higher in EAC than in ESCC, as well as in BE or D vs. ESCC. Interestingly, mean CDH13 NMV was significantly lower in short-segment than in long-segment BE, a known clinical risk factor for neoplastic progression. Similarly, BE segment length was significantly lower in specimens with unmethylated than with methylated CDH13 promoters. 5-aza-2'-deoxycytidine treatment of OE33 EAC and KYSE220 ESCC cells reduced CDH13 methylation and increased CDH13 mRNA expression. These findings suggest that hypermethylation of CDH13 is a common, tissue-specific event in human EAC, occurs early during BE-associated neoplastic progression, and correlates with known clinical neoplastic progression risk factors.

64 citations


Authors

Showing all 5043 results

NameH-indexPapersCitations
Shizuo Akira2611308320561
James G. Fujimoto1651115116451
Kiyoshi Takeda129416109817
David A. Brenner12849952756
Akira Yamamoto117199974961
Osamu Takeuchi11628890116
Takaomi C. Saido9035227802
Taroh Kinoshita8737923714
Takenobu Kamada8670027535
Kazuhiko Nakagawa8491741018
Takashi Yamamoto84140135169
Taro Kawai8314166916
Hiroo Imura8378129276
Kunio Matsumoto8246525131
Yukihiko Kitamura8041937965
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20232
202229
2021669
2020558
2019565
2018551