経皮経肝胆道鏡 percutaneous transhepatic cholangioscopy

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1. 経皮経肝胆道鏡検査 percutaneous transhepatic cholangioscopy
2. ルー・ワイ吻合術実施患者におけるERCP ercp in patients with roux en y anatomy
3. 再発性化膿性胆管炎 recurrent pyogenic cholangitis
4. 腎同種移植片のC4d染色および抗体媒介性拒絶反応の治療 c4d staining in renal allografts and treatment of antibody mediated rejection
5. 胆石治療のためのレーザー砕石術 laser lithotripsy for the treatment of gallstones

English Journal

PRDX1 and PRDX6 are repressed in papillary thyroid carcinomas via BRAF V600E-dependent and -independent mechanisms.

Nicolussi A1, D'Inzeo S1, Mincione G2, Buffone A3, Di Marcantonio MC2, Cotellese R2, Cichella A2, Capalbo C3, Di Gioia C4, Nardi F4, Giannini G3, Coppa A1.Author information 1Department of Experimental Medicine, Sapienza University of Rome, Rome, Italy.2Department of Experimental and Clinical Sciences, 'G. d'Annunzio' University Foundation, Chieti-Pescara, Italy.3Department of Molecular Medicine, Sapienza University of Rome, Rome, Italy.4Department of Radiological, Oncological and Pathological Sciences, Sapienza University of Rome, Rome, Italy.AbstractMany clinical studies highlight the dichotomous role of PRDXs in human cancers, where they can exhibit strong tumor-suppressive or tumor-promoting functions. Recent evidence suggests that lower expression of PRDXs correlates with cancer progression in colorectal cancer (CRC) or in esophageal squamous carcinoma. In the thyroid, increased levels of PRDX1 has been described in follicular adenomas and carcinomas, as well as in thyroiditis, while reduced levels of PRDX6 has been found in follicular adenomas. We studied the expression of PRDX1 and PRDX6, in a series of thyroid tissue samples, covering different thyroid diseases, including 13 papillary thyroid carcinomas (PTCs). Our results show that PRDX1 and PRDX6 are significantly reduced in all PTCs compared to normal tissues, to non-neoplastic tissue (MNG) or follicular neoplasms. This reduction is strongly evident in PTCs harboring BRAF V600E (31% of our cases). Using TPC-1 and BCPAP and FRTL-5 cell lines, we demonstrate for the first time that the presence of BRAF V600E is responsible of the hypoexpression of PRDX1 and PRDX6 both at mRNA and protein levels. Finally, independently of BRAF status, we observe an interesting correlation between the tumor size, the presence of lymph node metastasis and the lowest PRDX1 and PRDX6 levels. Therefore, these data indicate that PRDX1 and PRDX6 expression not only may play a key role in papillary thyroid carcinogenesis via a BRAF V600E-dependent mechanism, but their determination could be considered as potential tumor marker for indicating tumor progression in PTCs, independently of BRAF status.
International journal of oncology.Int J Oncol.2014 Feb;44(2):548-56. doi: 10.3892/ijo.2013.2208. Epub 2013 Dec 5.
Many clinical studies highlight the dichotomous role of PRDXs in human cancers, where they can exhibit strong tumor-suppressive or tumor-promoting functions. Recent evidence suggests that lower expression of PRDXs correlates with cancer progression in colorectal cancer (CRC) or in esophageal squamou
PMID 24316730

A subset of papillary thyroid carcinomas contain KRAS mutant subpopulations at levels above normal thyroid.

Myers MB, McKim KL, Parsons BL.Author information Division of Genetic and Molecular Toxicology, National Center for Toxicological Research, U.S. Food and Drug Administration, Jefferson, Arkansas.AbstractThe molecular pathogenesis of papillary thyroid carcinoma (PTC) is largely attributed to chromosomal rearrangements and point mutations in genes within the MAPK pathway (i.e., BRAF and RAS). Despite KRAS being the 6th most frequently mutated gene for all cancers, the reported frequency in thyroid cancer is only 2%. This may be due, in part, to the use of insensitive mutation detection methods such as DNA sequencing. Therefore, using the sensitive and quantitative ACB-PCR approach, we quantified KRAS codon 12 GGT → GAT and GGT → GTT mutant fraction (MF) in 20 normal thyroid tissues, 17 primary PTC, 2 metastatic PTC, and 1 anaplastic thyroid carcinoma. We observed measurable levels of KRAS codon 12 GAT or GTT mutation in all normal thyroid tissues. For PTCs, 29.4% and 35.3% had KRAS codon 12 GAT and GTT MF above the 95% upper confidence interval for the corresponding MFs in normal thyroid. The highest observed KRAS codon 12 GTT MFs were associated with tumors with follicular characteristics and relatively high levels of tumor necrosis. The results indicate KRAS mutant subpopulations are present in a large number of thyroid tumors, a fact previously unrecognized. The presence of KRAS mutation may indicate a tumor with an aggressive phenotype, thus directing the course of clinical treatment. © 2012 Wiley Periodicals, Inc.
Molecular carcinogenesis.Mol Carcinog.2014 Feb;53(2):159-67. doi: 10.1002/mc.21953. Epub 2012 Aug 28.
The molecular pathogenesis of papillary thyroid carcinoma (PTC) is largely attributed to chromosomal rearrangements and point mutations in genes within the MAPK pathway (i.e., BRAF and RAS). Despite KRAS being the 6th most frequently mutated gene for all cancers, the reported frequency in thyroid ca
PMID 22930660

Short term exposure to elevated levels of leptin reduces proximal tubule cell metabolic activity.

Briffa JF, Grinfeld E, McAinch AJ, Poronnik P, Hryciw DH.Author information Biomedical and Lifestyle Diseases (BioLED) Unit, College of Health and Biomedicine, Victoria University, St Albans, VIC 3021, Australia; Department of Physiology, The University of Melbourne, Parkville, VIC 3010, Australia.AbstractLeptin plays a pathophysiological role in the kidney, however, its acute effects on the proximal tubule cells (PTCs) are unknown. In opossum kidney (OK) cells in vitro, Western blot analysis identified that exposure to leptin increases the phosphorylation of the mitogen-activated protein kinase (MAPK) p44/42 and the mammalian target of rapamycin (mTOR). Importantly leptin (0.05, 0.10, 0.25 and 0.50 μg/ml) significantly reduced the metabolic activity of PTCs, and significantly decreased protein content per cell. Investigation of the role of p44/42 and mTOR on metabolic activity and protein content per cell, demonstrated that in the presence of MAPK inhibitor U0126 and mTOR inhibitor Ku-63794, that the mTOR pathway is responsible for the reduction in PTC metabolic activity in response to leptin. However, p44/42 and mTOR play no role the reduced protein content per cell in OKs exposed to leptin. Therefore, leptin modulates metabolic activity in PTCs via an mTOR regulated pathway.
Molecular and cellular endocrinology.Mol Cell Endocrinol.2014 Jan 25;382(1):38-45. doi: 10.1016/j.mce.2013.09.001. Epub 2013 Sep 12.
Leptin plays a pathophysiological role in the kidney, however, its acute effects on the proximal tubule cells (PTCs) are unknown. In opossum kidney (OK) cells in vitro, Western blot analysis identified that exposure to leptin increases the phosphorylation of the mitogen-activated protein kinase (MAP
PMID 24036423

Japanese Journal

経皮経肝胆道鏡による結石治療のコツ

三好広尚,乾和郎,芳野純治
日本消化器内視鏡学会雑誌 = Gastroenterological endoscopy 53(7), 1818-1827, 2011-07-20
… PTCSによる結石治療のコツについて解説した．PTCSは総胆管結石および肝内結石に有用な治療法である．PTCSはERCP関連手技による治療が困難な場合に適応となる非手術的な治療法である．PTCSによる結石治療のポイントとしては(1)PTCSによる結石治療の適応，(2)PTBDの挿入と拡張，(3)PTCSによる結石除去，(4)結石除去後の …
NAID 10029562526

Long-term survival of over 4 years after microwave tissue coagulation (MTC) therapy via percutaneous transhepatic cholangioscopy in men with jaundice and bile duct carcinoma in the far advanced stage

Ino-u-e Shigeaki,Endoh Masaaki,Fukushima Takashi,Nakadate Toshihiro,Karouji Sinobu,Shioya Akira,Ohsato Masayuki,Itoh Takao,Shida Shoichi,Nakachi Hiromichi,Narumi Syunnji,Hakamada Kennichi,Sasaki Mutsuo,Ebina Yuuichi,Umehara Yutaka,Andoh Hideaki,Fukuyama Shouji,Hatazawa Chiaki,Segami Hideo,Konn Mitsuru,Seki Toshihito,Tabuse Katsuyoshi
Journal of Microwave Surgery 29(0), 51-57, 2011
… cases of 2 jaundice patients with bile duct carcinoma in the far advanced stage of progression, who survived for more than 4 years after percutaneous transhepatic cholangioscopy (PTCS) and radiography-guided MTC.Long-term survival of over 10 years was achieved in jaundice patients with unresectable bile duct carcinoma and poor health after performing PTCS and radiography-guided MTC.MTC may be an alternative palliative treatment for jaundice patients in the far advanced stage of progression and may afford survival of over 4 …
NAID 130001157660