KOL | YUKISATO KITAMURADepartment of Pathobiological Science and Technology, School of Health Science, Tottori University Faculty of Medicine, Yonago, Japan. | Department of Pathobiological Science ... |
KOL Resume for YUKISATO KITAMURA
| Year | |
|---|---|
| 2019 | Department of Pathobiological Science and Technology, School of Health Science, Tottori University Faculty of Medicine, Yonago, Japan. |
| 2018 | Department of Pathobiological Science and Technology, School of Health Science, Tottori University Faculty of Medicine, Yonago 683-8503, Japan. Electronic address: |
| 2017 | Department of Pathobiological Science and Technology, School of Health Science, Tottori University Faculty of Medicine, Yonago 683-8503, Japan. |
| 2014 | Department of Pathobiological Science and Technology, School of Health Science, Tottori University Faculty of Medicine, Yonago, Japan |
| 2012 | Division of Molecular Pathology, Department of Pathology, Department of Pathobiological Science and Technology, School of Health Science, and, Division of Dermatology, Tottori University Faculty of Medicine, and, Department of Pathology, Tottori University Hospital, Yonago, Japan |
| 2008 | Division of Molecular Pathology, Department of Microbiology and Pathology, Tottori University, Departments of |
| 2007 | Pathology, Tottori University Faculty of Medicine, Yonago 683-8503, Japan, Divisions of Molecular Pathology and |
| 2006 | Division of Molecular Pathology, Department of Microbiology and Pathology, Tottori University Faculty of Medicine, Yonago, Japan Department of Microbiology and Pathology, Tottori University and Departments of |
| 2005 | From the Division of Pathology, Department of Pathology and Microbiology, Tottori University Faculty of Medicine, Yonago, Japan (Drs Hayashi, Takahata, Adachi, and Kitamura); and Tottori University Hospital, Yonago, Japan (Drs Horie and Kato) |
| 2003 | Second Department of Pathology and |
| 2002 | Department of Pathology, Tottori University Faculty of Medicine, Yonago 683,Japan |
| 2001 | Second Department of Pathology, Faculty of Medicine |
| 2000 | Second Department of Pathology, Faculty of Medicine and |
| 1999 | Second Department of Pathology, Tottori University, Yonago, Japan |
| 1998 | †Second Department of Pathology, Tottori University School of Medicine, Yonago, Japan |
| 1997 | The Second Department of Pathology, Tottori University, Facuty of Medicine |
| 1996 | Department of Pathology, Faculty of Medicine, Tottori University, Tottori 680, Japan |
| 1995 | Tottori Univ, Fac Med, Dept Pathol 2, Yonago, Tottori 683, Japan; Tottori Univ, Fac Med, Dept Bacteriol, Yonago, Tottori 683, Japan; Tottori Univ, Fac Med, Inst Neurol Sci, Div Child Neurol, Yonago, Tottori 683, Japan; Tottori Univ, Fac Med, Dept Pathol 1, Yonago, Tottori 683, Japan and Tottori Univ, Fac Med, Dept Med Zool, Yonago, Tottori 683, Japan |
YUKISATO KITAMURA: Influence Statistics
| Concept | World rank |
|---|---|
| surgical resected appendix | #2 |
| tgf beta1 hsc | #2 |
| smad signalings hsc | #2 |
| nucleus tgfbeta1 stimulation | #2 |
| signalings tgf | #2 |
| appendix pcr | #2 |
| tcell lymphoma appendix | #2 |
| tgfbeta1 stimulation increase | #2 |
| weak cirrhotic | #2 |
| strong smad expression | #2 |
| ultra echo sonograph | #2 |
| lymphoma cell monoclonality | #2 |
| 84yearold female appendectomy | #2 |
| tcell mcburney | #2 |
| appendectomy result | #2 |
| nucleus hsc | #2 |
| increase smad expressions | #2 |
| hsc cirrhotic liver | #2 |
| strong smad | #2 |
| signalings hsc | #2 |
| exon procollagen | #3 |
| mcpyvlarge tantigen | #3 |
| aso inhibitory effects | #3 |
| lipofection immunohistochemistry | #3 |
| diffused proliferation | #3 |
| region junctional region | #3 |
| complementary junctional | #3 |
| aug aso | #3 |
| cutaneous hpvdna | #3 |
| polyomaviruses mucosal | #3 |
| hsc aso | #3 |
| junctional region intron | #3 |
| junctional region effects | #3 |
| exon junctional region | #3 |
| aso complementary exon | #3 |
| patient report analyses | #3 |
| complementary aso | #3 |
| exon aso complementary | #3 |
| blotting inhibitory | #3 |
| autocrine tgf beta1 | #3 |
| lipofection aso | #3 |
| 6 human polyomaviruses | #3 |
| inhibitory effects aso | #3 |
| aso complementary aug | #3 |
| aso inhibitory | #3 |
| analyses skin cancer | #3 |
| transplantrelated skin tumor | #3 |
| aso aug | #3 |
| aug intron | #3 |
| effects aso complementary | #3 |
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Prominent publications by YUKISATO KITAMURA
Immunolocalization of E-cadherin (E-cad), alpha-catenin, beta-catenin, and CD44 has rarely been investigated in human cholangiocarcinoma (CC). We, therefore, immunohistochemically examined the expression of E-cad, alpha-catenin, beta-catenin, CD44 standard (CD44s), and CD44 variants (CD44v) including CD44v5, CD44v6, CD44v7-8, and CD44v10 in normal adult livers and in 47 cases of CC; and the results were then correlated with tumor grade, vascular invasion, metastasis, p53 expression, ...
| Known for Human Cholangiocarcinoma | Catenin Expression | Immunohistochemical Study | Tumor Grade | Vascular Invasion |
Merkel cell carcinoma (MCC) is a rare, aggressive neuroendocrine skin cancer, with approximately 80% of cases related to Merkel cell polyomavirus (MCPyV). Indoleamine 2,3-dioxygenase 1 (IDO1) and tryptophan 2,3-dioxygenase 2 (TDO2) are the key rate-limiting enzymes of the tryptophan-to-kynurenine metabolic pathway. With aryl hydrocarbon receptor (AhR), an intracellular transcription factor, they play a role in escaping the immunosurveillance process in several cancers. IDO1/TDO2/AhR ...
| Known for Merkel Cell | Ido1 Expression | Tumor Microenvironment | Carcinoma Mcc | Mcpyv Negative |
In lung cancers, lymph node metastasis of cancer cells is one of the most important prognostic factors, and lymphatic vessel invasion (LVI) is very important in the stage preceding lymph node metastases. Recently, it has been reported that lymphatic vessel density (LVD) is associated with lymph node metastasis. The aim of the present study was to evaluate the relationship between LVD and LVI based on the immunohistochemical expression of podoplanin or D2-40, which are new specific ...
| Known for Lymph Node | Murinederived Biomarkers | Monoclonal Antibodies | Vessel Density | Cancer Cells |
Tissue inhibitor of metalloproteinase-1 in the liver of patients with chronic liver disease
[ PUBLICATION ]
BACKGROUND/AIMS: Tissue inhibitor of metalloproteinase (TIMP)-1 is an important regulator of matrix metalloproteinase activity. To clarify the changes in TIMP-1 in diseased livers, we measured TIMP-1 concentrations in liver tissue samples from patients with chronic liver disease. The relationship between serum and liver levels of TIMP-1 was also examined in some patients.
METHODS: The subjects were 68 patients who underwent liver biopsy. The liver TIMP-1 concentration was measured using ...
| Known for Liver Disease | Tissue Inhibitor | Hepatitis Chronic | Serum Timp1 | Periportal Necrosis |
Niemann-Pick disease type C (NPC) is an inherited lipid storage disorder caused by mutations in NPC1 or NPC2 genes. Loss of function of either protein results in the endosomal accumulation of cholesterol and other lipids, progressive neurodegeneration, and robust glial cell activation. Here, we report that cultured human NPC fibroblasts secrete interferon-beta, interleukin-6 (IL-6), and IL-8, and contain increased levels of signal transducers and activators of transcription (STATs). ...
| Known for Pick Disease | Receptor 4 | Endosomal Accumulation | Glial Cells | Npc1 Mice |
Smad expression of hepatic stellate cells in liver cirrhosis in vivo and hepatic stellate cell line in vitro
[ PUBLICATION ]
Smad expressions, signaling mediators of transforming growth factor-beta (TGF-beta) superfamily of cytokines, were investigated in paraffin-embedded tissue sections of liver cirrhosis due to the hepatitis C virus infection and in the hepatic stellate cell (HSC) line in vitro. Smad 2/3, 4 and 7 was expressed in the nucleus of the HSC in the cirrhotic liver, while the expression was weak in the non-cirrhotic liver. TGF-beta1 expression in the HSC of the cirrhotic liver was strong, while ...
| Known for Smad Expression | Liver Cirrhosis | Hepatic Stellate | Tgfbeta1 Stimulation | Situ Hybridization |
Detection of Merkel Cell Polyomavirus in the Human Tissues from 41 Japanese Autopsy Cases Using Polymerase Chain Reaction
[ PUBLICATION ]
It has recently been shown that approximately 80% of Merkel cell carcinomas harbor a novel polyomavirus named Merkel cell polyomavirus (MCPyV). MCPyV has been detected in human tissue samples. However, detailed distribution of MCPyV in non-neoplastic Japanese human tissues remains unclear. To address this, we used single or real-time quantitative polymerase chain reaction (PCR) for 41 autopsy cases. PCR revealed MCPyV-DNA in non-neoplastic samples: total, 29/41 (71%); adult, 29/39 (74%); ...
| Known for Merkel Cell | Polymerase Chain | Viral Load | Polyomavirus Mcpyv | Bone Marrow |
Absence of mutations in the β‐catenin and adenomatous polyposis coli genes in papillary and follicular thyroid carcinomas
[ PUBLICATION ]
beta-Catenin has multiple functions both in intercellular adhesion and in signal transduction. As a signaling molecule, mutations in exon 3 of the beta-catenin gene stabilize this protein in the cytoplasm. Subsequently, accumulated beta-catenin protein translocates to nuclei with T-cell factor-4, and upregulates transcriptional activity of the target genes involved in carcinogenesis. Mutations in exon 3 of the beta-catenin gene have been detected in various carcinomas. We examined ...
| Known for Follicular Thyroid | Beta Catenin | Papillary Carcinoma | Adenomatous Polyposis | Target Genes |
Association of expression of the hedgehog signal with Merkel cell polyomavirus infection and prognosis of Merkel cell carcinoma
[ PUBLICATION ]
Merkel cell carcinoma (MCC) is an aggressive neuroendocrine skin cancer that mostly occurs in the elderly. Merkel cell polyomavirus (MCPyV) is detected in approximately 80% of MCCs and is associated with carcinogenesis. Hedgehog signaling pathway plays a role in human embryogenesis and organogenesis. In addition, reactivation of this pathway later in life can cause tumors. Twenty-nineMCPyV-positive and 21 MCPyV-negative MCCs were immunohistochemically stained with primary antibodies for ...
| Known for Merkel Cell | Tumor Carcinoma | Mcpyvnegative Mccs | Expression Hedgehog | Polyomavirus Mcpyv |
BACKGROUND/AIMS: Cell adhesion molecules play an important role in the morphogenesis of developing organs. However, little is known about their expression during intrahepatic bile duct development.
METHODS: We immunohistochemically investigated the expression of E-cadherin (E-Cad), alpha-catenin (A-Cat) and beta-catenin (B-Cat) during human intrahepatic bile duct development, using 31 fetal livers of various gestational ages. The developmental stages of bile ducts were classified into ...
| Known for Intrahepatic Bile | Ductal Plate | Fetal Development | Biliary Cells | Beta Catenin |
According to the World Health Organization classification, neoplasms with perivascular epithelioid cell differentiation (PEComas) are mesenchymal tumors composed of histologically and immunohistochemically distinctive PEC. Generally, nearly all PEComas have immunoreactivity for both melanocytic (HMB-45 and/or melan A) and smooth muscle (actin (SMA) and/or desmin) markers. Recently the authors reported that benign clear cell sugar tumor of the lung, one of the PEComas, expressed CD1a. ...
| Known for Cd1a Expression | Cd1 Biomarkers | Soft Tissue | Mesenchymal Tumors | Epithelioid Cell |
Most adults have persistent Epstein-Barr virus (EBV)-infection. Adolescents and young adults with primary EBV-infection frequently develop infectious mononucleosis. Latent EBV-infection is associated with various diseases, neoplasms, and hematological disorders. In vivo animal models of human EBV infection, such as non-human primates, have had limited success. A new rabbit model for primary human EBV-infection is described in this study. Seven male rabbits inoculated intravenously with ...
| Known for Barr Virus | Human Ebv | Animal Model | Pathological Analysis | Viral Rabbits |
We have earlier shown that dystroglycan (DG) is a lamininbinding protein and as such is a cell adhesion molecule. DG is a heterodimer of alpha and beta DG subunits. beta-dystroglycan (betaDG) is the membrane spanning subunit, whereas the alpha subunit is bound to the extracellular domain of betaDG. To study physiological function of the protein, we expressed full-length DG (FL-DG) and the cytoplasmic domain of betaDG (deltabetaDG) in bovine aortic endothelial cells (BAE) and examined ...
| Known for Endothelial Cells | Cell Adhesion | Dystroglycan Dg | Cytoplasmic Domain | Lamininbinding Protein |
Key People For Merkel Cell
YUKISATO KITAMURA:Expert Impact
Concepts for whichYUKISATO KITAMURAhas direct influence:Merkel cell, Situ hybridization, Merkel cell polyomavirus, Cd1a expression, Cell polyomavirus, Merkel cell carcinoma, Inhibitory effects, Cell carcinoma.
YUKISATO KITAMURA:KOL impact
Concepts related to the work of other authors for whichfor which YUKISATO KITAMURA has influence:Liver fibrosis, Merkel cell, Chronic hepatitis, Growth factor, Intrahepatic cholangiocarcinoma, Tissue inhibitor, Biliary tract.
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