Institution
Kanazawa Medical University
Education•Kanazawa, Japan•
About: Kanazawa Medical University is a education organization based out in Kanazawa, Japan. It is known for research contribution in the topics: Population & Cancer. The organization has 3103 authors who have published 6322 publications receiving 144592 citations. The organization is also known as: Kanazawa ika daigaku.
Topics: Population, Cancer, Diabetes mellitus, Lung cancer, Blood pressure
Papers published on a yearly basis
Papers
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TL;DR: It is vitally important for the further development to establish standards for ‘zheng’ of CFS, to perform randomized and controlled trials of TCM on CFS and to make full use of the latest biological, biochemical, molecular and immunological approaches in the experimental design.
Abstract: More and more patients have been diagnosed as having chronic fatigue syndrome (CFS) in recent years. Western drug use for this syndrome is often associated with many side-effects and little clinical benefit. As an alternative medicine, traditional Chinese medicine (TCM) has provided some evidences based upon ancient texts and recent studies, not only to offer clinical benefit but also offer insights into their mechanisms of action. It has perceived advantages such as being natural, effective and safe to ameliorate symptoms of CFS such as fatigue, disordered sleep, cognitive handicaps and other complex complaints, although there are some limitations regarding the diagnostic standards and methodology in related clinical or experimental studies. Modern mechanisms of TCM on CFS mainly focus on adjusting immune dysfunction, regulating abnormal activity in the hypothalamic-pituitary-adrenal (HPA) axis and serving as an antioxidant. It is vitally important for the further development to establish standards for ‘zheng’ of CFS, i.e. the different types of CFS pathogenesis in TCM, to perform randomized and controlled trials of TCM on CFS and to make full use of the latest biological, biochemical, molecular and immunological approaches in the experimental design.
63 citations
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TL;DR: It is suggested that pitavastatin attenuates chronic inflammation and improves the imbalance of adipocytokines, both of which are caused by the presence of excess adipose tissues, thereby preventing the development of colonic premalignancies in an obesity‐related colon cancer model.
Abstract: Obesity and related metabolic abnormalities are risk factors for colorectal cancer. A state of chronic inflammation and adipocytokine imbalance may play a role in colorectal carcinogenesis. Statins, which are commonly used for the treatment of hyperlipidemia, are known to possess anti-inflammatory effects. Statins also exert chemopreventive properties against various cancers. The present study examined the effects of pitavastatin, a recently developed lipophilic statin, on the development of azoxymethane (AOM)-initiated colonic premalignant lesions in C57BL/KsJ-db/db (db/db) obese mice. Male db/db mice were administrated weekly subcutaneous injections of AOM (15 mg/kg body weight) for 4 weeks and then were subsequently fed a diet containing 1 ppm or 10 ppm pitavastatin for 8 weeks. Feeding with either dose of pitavastatin significantly reduced the number of colonic premalignant lesions, beta-catenin accumulated crypts, by inhibiting proliferation and the surrounding inflammation. Pitavastatin increased the serum levels of adiponectin while conversely decreasing the serum levels of total cholesterol, tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, IL-18, and leptin. Pitavastatin also caused a significant increase in the expression of phosphorylated form of the AMP-activated kinase (AMPK) protein on the colonic mucosa of AOM-treated mice. In addition, the expression levels of TNF-alpha, IL-6, IL-18, and COX-2 mRNAs on the colonic mucosa of AOM-treated mice were decreased by treatment with this agent. These findings suggest that pitavastatin attenuates chronic inflammation and improves the imbalance of adipocytokines, both of which are caused by the presence of excess adipose tissues, thereby preventing the development of colonic premalignancies in an obesity-related colon cancer model. Therefore, some types of statins, including pitavastatin, may be a useful chemoprevention modality for colon cancer in obese individuals.
63 citations
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TL;DR: It is suggested that alcohol altered liver membrane antibody is a factor related to the progression of alcoholic liver disease and that hepatitis C virus infection is a determining factor for development of hepatocellular carcinoma and for prognosis of cirrhosis in patients who continue to drink.
63 citations
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TL;DR: The hepatokine SeP may be a novel therapeutic target for impaired angiogenesis in type 2 diabetes after treatment with glucose increased gene expression and transcriptional activity for Sepp1 in H4IIEC hepatocytes.
Abstract: Impaired angiogenesis induced by vascular endothelial growth factor (VEGF) resistance is a hallmark of vascular complications in type 2 diabetes; however, its molecular mechanism is not fully understood. We have previously identified selenoprotein P (SeP, encoded by the SEPP1 gene in humans) as a liver-derived secretory protein that induces insulin resistance. Levels of serum SeP and hepatic expression of SEPP1 are elevated in type 2 diabetes. Here, we investigated the effects of SeP on VEGF signalling and angiogenesis. We assessed the action of glucose on Sepp1 expression in cultured hepatocytes. We examined the actions of SeP on VEGF signalling and VEGF-induced angiogenesis in HUVECs. We assessed wound healing in mice with hepatic SeP overexpression or SeP deletion. The blood flow recovery after ischaemia was also examined by using hindlimb ischaemia model with Sepp1-heterozygous-knockout mice. Treatment with glucose increased gene expression and transcriptional activity for Sepp1 in H4IIEC hepatocytes. Physiological concentrations of SeP inhibited VEGF-stimulated cell proliferation, tubule formation and migration in HUVECs. SeP suppressed VEGF-induced reactive oxygen species (ROS) generation and phosphorylation of VEGF receptor 2 (VEGFR2) and extracellular signal-regulated kinase 1/2 (ERK1/2) in HUVECs. Wound closure was impaired in the mice overexpressing Sepp1, whereas it was improved in SeP
−/−mice. SeP
+/−mice showed an increase in blood flow recovery and vascular endothelial cells after hindlimb ischaemia. The hepatokine SeP may be a novel therapeutic target for impaired angiogenesis in type 2 diabetes.
63 citations
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TL;DR: Six species of Sporothrix schenckii showed unique restriction profiles which could be discriminated from each other and were separated into 7 types based on restriction profile heterogeneity.
Abstract: Restriction profiles by HaeIII of mitochondrial DNA were studied for classification and distinction of Sporothrix schenckii (100 strains), S. schenckii var. luriei (1), S. curviconia (1), S. inflata (7), Ceratocystis stenoceras (17) and C. minor (7). These 6 species showed unique restriction profiles which could be discriminated from each other. S. schenckii was further separable into 11 types, S. inflata into 4 types, C. stenoceras into 4 types and C. minor into 7 types based on restriction profile heterogeneity.
63 citations
Authors
Showing all 3113 results
Name | H-index | Papers | Citations |
---|---|---|---|
Michael Marmot | 193 | 1147 | 170338 |
Tadamitsu Kishimoto | 181 | 1067 | 130860 |
Masayuki Yamamoto | 171 | 1576 | 123028 |
Zena Werb | 168 | 473 | 122629 |
Toshio Hirano | 120 | 401 | 55721 |
John T. Isaacs | 88 | 356 | 28217 |
Hiroshi Sasaki | 76 | 644 | 24222 |
Takuji Tanaka | 75 | 490 | 20946 |
Hiroshi Shimizu | 71 | 1368 | 26668 |
Daisuke Koya | 67 | 294 | 18746 |
Masashi Tanaka | 65 | 396 | 17110 |
Masashi Akiyama | 65 | 685 | 16404 |
Masayoshi Takeuchi | 64 | 279 | 13651 |
Takashi Yoshida | 63 | 328 | 13680 |
Tsutomu Hatano | 61 | 299 | 13668 |