Anonymization server system for DICOM images

We have developed an anonymization system for DICOM images. It requires consent from the patient to use the DICOM images for research or education. However, providing the DICOM image to the other facilities is not safe because it contains a lot of personal data. Our system is a server that provides anonymization service of DICOM images for users in the facility. The distinctive features of the system are, input interface, flexible anonymization policy, and automatic body part identification. In the first feature, we can use the anonymization service on the existing DICOM workstations. In the second feature, we can select a best policy fitting for the Protection of personal data that is ruled by each medical facility. In the third feature, we can identify the body parts that are included in the input image set, even if the set lacks the body part tag in DICOM header. We installed the system for the first time to a hospital in December 2005. Currently, the system is working in other four facilities. In this paper we describe the system and how it works

Prolonged oxidative stress and delayed tissue repair exacerbate acetaminophen-induced liver injury in aged mice

マウスにアセトアミノフェンを投与して急性劇症肝炎を誘導すると，中心静脈域にネクローシスによる大量の肝細胞死が誘導される．障害後は，速やかに障害が解消され，障害後48 時間後には活発な肝細胞増殖が誘導され，組織再生が進行する．老齢マウスでは，アセトアミノフェン代謝産物の処理能力低下による障害の持続，障害部位へのマクロファージ集積低下による死細胞の残存，肝細胞増殖能の低下，などによって障害の持続と再生の遅延が認められた．本研究の結果は，加齢が薬剤の肝毒性を高めるリスクファクターとなる場合があることを示している

Epigenetic inactivation of the LRFN5 gene encoding type I transmembrane glycoprotein in esophageal squamous cell carcinoma

Alcohol drinking and cigarette smoking are significantly associated with an increased risk of esophageal cancer. Promoter hypermethylation of tumor suppressor genes plays an important role in esophageal squamous cell carcinoma (ESCC). To profile methylation changes and to identify methylated genes in clinical ESCC samples in a high-throughput fashion, we carried out genomewide methylation analysis using the methylated CpG island amplifi cation microarray (MCAM) technique in paired samples of ESCC and adjacent non-cancerous tissue and normal esophageal mucosa. As a surrogate of genome-wide hypomethylation, levels of LINE-1 methylation were analyzed using bisulfi te pyrosequencing. The degree of genome-wide methylation of the majority of non-cancerous esophageal tissues was intermediate between that of ESCC tissues and that of normal esophageal mucosa of healthy volunteers. A total of 210 candidate genes that are hypermethylated in ESCCs were identifi ed by using the MCAM technique. Among the candidate genes, we found that the LRFN5 gene coding for a transmembrane protein was transcriptionally silenced by promoter CpG island hypermethylation in ESCC. LRFN5 CpG island hypermethylation was a relatively common event even in patients without drinking habits. LRFN5 expression levels were reduced in most of the ESCC cell lines and ESCC tissues, being correlated with hypemethylation.Methylation levels of LINE-1 were significantly lower in tumor tissues than in adjacent non-tumor tissues of ESCC and inversely correlated with LRFN5 methylation. Importantly, LRFN5 immunostaining was undetectable in 5/7 (71%) intramucosal ESCC tissues,suggesting that LRFN5 silencing is an early event in ESCC pathogenesis. Hypermethylation of the LRFN5 gene may provide a useful marker for detecting preinvasive and early-stage ESCC, especially in individuals without drinking habits.departmental bulletin pape

An automated distinction of DICOM image for lung cancer CAD system

Automated distinction of medical images is an important preprocessing in Computer-Aided Diagnosis (CAD) systems. The CAD systems have been developed using medical image sets with specific scan conditions and body parts. However, varied examinations are performed in medical sites. The specification of the examination is contained into DICOM textual meta information. Most DICOM textual meta information can be considered reliable, however the body part information cannot always be considered reliable. In this paper, we describe an automated distinction of DICOM images as a preprocessing for lung cancer CAD system. Our approach uses DICOM textual meta information and low cost image processing. Firstly, the textual meta information such as scan conditions of DICOM image is distinguished. Secondly, the DICOM image is set to distinguish the body parts which are identified by image processing. The identification of body parts is based on anatomical structure which is represented by features of three regions, body tissue, bone, and air. The method is effective to the practical use of lung cancer CAD system in medical sites

Activation of microRNA-596 induced by DNA demethylation and interferon in malignant melanoma cells

Dysregulation of microRNA has been implicated in melanoma, although the mechanism is not fully understood. We aimed to examine the epigenetically silenced miRNAs and its involvement in the antitumor effect of DNA demethylation and interferon in melanoma. Growth suppressive effects of 5-aza-2’deoxycytidine plus interferon-β were assessed in 20 melanoma cell lines, and the highest effect was observed in TXM18 cells. A screen for miRNAs induced by 5-aza-2’deoxycytidine plus IFN-β in TXM18 cells identifi ed a set of miRNAs including miR-7, miR-203, miR-215 and miR-596. The CpG island of the miR-596 gene was highly methylated in all melanoma cell lines tested (n = 20) whereas levels of methylation were limited in normal melanocytes. Methylation levels of miR-596 were signifi cantly higher in clinical specimens of melanoma than in benign melanocytic nevi (40.6% vs. 30.1%, P= 0.018). Furthermore, transfection of a precursor of miR-596 into melanoma cells induced growth suppression, indicating that the effect of 5-aza-2’deoxycytidine plus interferon-β is in part due to induction of miR-596. Our data suggest that miR-596 is a novel tumor suppressor frequently silenced by DNA methylation in melanoma; that modulation of miRNAs may be involved in the antitumor effect of DNA demethylation plus interferon in melanoma.departmental bulletin pape

Analysis of the anti-tumor mechanism of BRD4 inhibition in hepatocellular carcinoma

Bromodomain and extra terminal (BET) family proteins, which include BRD4, are readers of histone acetyl-lysines and key regulators of gene transcription. BRD4 inhibitors exert anti-tumor effects in various cancers, including hepatocellular carcinoma (HCC). We investigated the mechanism underlying the antitumor effects of BRD4 inhibition in HCC. We first tested the effects of the BRD4 inhibitor JQ1 in a series of 9 HCC cell lines and found that it strongly suppressed HCC cell proliferation by inducing cell cycle arrest and apoptosis. Gene expression microarray analysis revealed that JQ1 also induced marked changes in the gene expression profiles of HCC cells, and genes associated with cell cycle and apoptosis were significantly enriched among the affected genes. Notably, a number of cancer-related genes, including BCAT1, DDR1, GDF15, FANCD2, SENP1 and TYRO3, were strongly suppressed by JQ1 in HCC cells. We also confirmed BRD4 bound within the promoter regions of these genes, which suggests they are targets of BRD4 in HCC cells. JQ1 thus appears to exert its anti-tumor effects in HCC by suppressing multiple BRD4 target genes

Выращивание ремонтного молодняка кур при использовании пробиотических препаратов «Бацелл» и «Моноспорин»

Применение пробиотических препаратов с первых дней жизни цыплят позволит получить в дальнейшем здоровую птицу с высокой реализацией генетического потенциала