20 research outputs found
<Abstract of annual report>Detection of Polyamines by a New Enzymatic Differential Assay (5) : Studies on Polyamine in Blood of Patients with Genitourinary Malignant Diseases.
腎血管腫
腎血管腫4例を報告した.良性血管性腫瘍である腎血管腫は腎動脈造影でも必ずしも異常陰影を示さず, 診断は困難である.うち2例の海綿状血管腫摘出例はCTで, 造影剤増強効果をもたないlow-densityな腫瘤影を示した.しかし, 動脈造影で診断した2例はCTでは異常陰影を認めなかった.このように腎血管腫の動脈造影とCTは血管腫自体の構成血管成分により種々の像を呈するものと考えるFour cases of renal hemangioma are presented. Renal hemangioma is difficult to detect because this benign vascular tumor never demonstrates any abnormalities on renal arteriography. Computed tomography in two resected cases of cavernous hemangioma revealed a low-density mass without any enhance effect, while the others diagnosed by the selective renal arteriography demonstrated no abnormality on computed tomography. We postulate that both angiographic and computed tomographic appearances of the renal hemangioma could depend on its vascular components. Related reports are also reviewed
Effects of Localized Distribution of Terminals and Mobility on Performance Improvement by Direct Communication
The Efficacy of Early Treatment of Seasonal Allergic Rhinitis with Benifuuki Green Tea Containing O-methylated Catechin before Pollen Exposure: An Open Randomized Study
Background: We previously reported that 'benifuuki' green tea containing O-methylated catechin significantly relieved the symptoms of perennial or seasonal rhinitis compared with a placebo green tea that did not contain O-methylated catechin in randomized double-blind clinical trials. In this study we assessed the effects of 'benifuuki' green tea on clinical symptoms of seasonal allergic rhinitis.
Methods: An open-label, single-dose, randomized, parallel-group study was performed on 38 subjects with Japanese cedar pollinosis. The subjects were randomly assigned to long-term (December 27, 2006 – April 8, 2007, 1.5 months before pollen exposure) or short-term (February 15, 2007: after cedar pollen dispersal – April 8, 2007) drinking of a 'benifuuki' tea drink containing 34 mg O-methylated catechin per day. Each subject recorded their daily symptom scores in a diary. The primary efficacy variable was the mean weekly nasal symptom medication score during the study period.
Results: The nasal symptom medication score in the long-term intake group was significantly lower than that of the short-term intake group at the peak of pollen dispersal. The symptom scores for throat pain, nose-blowing, tears, and hindrance to activities of daily living were significantly better in the long-term group than the short-term group. In particular, the differences in the symptom scores for throat pain and nose-blowing between the 2 groups were marked.
Conclusions: We conclude that drinking 'benifuuki' tea for 1.5 months prior to the cedar pollen season is effective in reducing symptom scores for Japanese cedar pollinosis
<Abstract of annual report>Detection of Polyamines by a New Enzymatic Differential Assay (5) : Studies on Polyamine in Blood of Patients with Genitourinary Malignant Diseases.
The annual rate of coronary artery calcification with combination therapy with a PCSK9 inhibitor and a statin is lower than that with statin monotherapy
Coronary artery calcification: entry to new frontier of PCSK9 inhibitors Today, rapid aging in society is making progress in developed countries. One of the most serious health problems in an aging society is atherosclerosis, of which final phase is coronary artery calcification (CAC). CAC could increase the risk of complications during coronary catheterization and coronary artery bypass surgery as well as ischemic heart disease (IHD). We, members in the aging society, would see much more patients with CAC in the near future. We, however, have no medications for CAC today. Moreover, statins that are used in the world have been known for CAC formation after long-term use. The team led by Yuichi Ikegami and Ikuo Inoue in Japan’s Saitama Medical University found that CAC in patients with atherosclerosis is improved by PCSK9 inhibitors compared to statins by using coronary computed tomographic angiography. This study shows us a hint that could lead us to new preventive therapies of IHD
A Novel Splicing Variant of Peroxisome Proliferator-Activated Receptor-γ (<i>Pparγ1sv</i>) Cooperatively Regulates Adipocyte Differentiation with <i>Pparγ2</i>
<div><p>Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors that regulate expression of a number of genes associated with the cellular differentiation and development. Here, we show the abundant and ubiquitous expression of a newly identified splicing variant of mouse <i>Pparγ</i> (<i>Pparγ1sv</i>) that encodes PPARγ1 protein, and its importance in adipogenesis. The novel splicing variant has a unique 5′-UTR sequence, relative to those of <i>Pparγ1</i> and <i>Pparγ2</i> mRNAs, indicating the presence of a novel transcriptional initiation site and promoter for <i>Pparγ</i> expression. <i>Pparγ1sv</i> was highly expressed in the white and brown adipose tissues at levels comparable to <i>Pparγ2</i>. <i>Pparγ1sv</i> was synergistically up-regulated with <i>Pparγ2</i> during adipocyte differentiation of 3T3-L1 cells and mouse primary cultured preadipocytes. Inhibition of <i>Pparγ1sv</i> by specific siRNAs completely abolished the induced adipogenesis in 3T3-L1 cells. C/EBPβ and C/EBPδ activated both the <i>Pparγ1sv</i> and <i>Pparγ2</i> promoters in 3T3-L1 preadipocytes. These findings suggest that <i>Pparγ1sv</i> and <i>Pparγ2</i> synergistically regulate the early stage of the adipocyte differentiation.</p></div
Effect of knock-down of <i>Pparγ1sv</i> on adipogenesis of 3T3-L1 cells.
<p>(A) Locations of the targeting sites of siRNAs for <i>Pparγ1sv</i>, <i>Pparγ2</i>, and both transcripts (common). For the validation of siRNAs using a luciferase reporter gene, the full-length <i>Pparγ1sv</i> or <i>Pparγ2</i> cDNA was inserted into <i>Xho</i> I site in pGL3-Control in sense or antisense direction. (B) Evaluation of siRNAs for <i>Pparγ1sv</i> or <i>Pparγ2</i>. 3T3-L1 cells were transfected with each of siRNA, and subjected to adipogenic induction in the following day (day 0). Expression of PPARγ1 and PPARγ2 proteins at day 2 was detected using PPARγ antibody with Lamin B1 as a control for nuclear extracts. siControl is negative control siRNA. Arrows indicate the positions of PPARγ1 and PPARγ2 proteins. (C) Validation of siRNA specificity. The relative luciferase activities were obtained from 3T3-L1 cells 1 day after transfection with pGL3-Control containing the <i>Pparγ1sv</i> or <i>Pparγ2</i> cDNA in sense or antisense direction and each of two respective siRNAs for <i>Pparγ1sv</i> and <i>Pparγ2</i>. The values represent the mean of triplicate measurements. The activity of siControl cells is defined as 100%. (D) 3T3-L1 cells transfected with siRNAs were subjected to adipogenic induction and stained by Oil Red O at day 9. Microscopic (x100) observations are shown. (E) Quantitative measurement of intracellular triglycerides in siRNA knock-down cells at days 0 and 6 using AdipoRed reagent. Data represent the mean of 4 replicate assays. *<i>P</i><0.01 compared to siControl cells at day 6. (F) Protein expression levels of PPARγ, C/EBPβ, C/EBPα, Lamin B1 (control for nuclear extracts), FABP4 (aP2), DLK (pref-1), and α-tubulin (control for cytosolic extracts) in <i>Pparγ1sv</i> or <i>Pparγ2</i> knock-down cells at days 2 and 6 detected by the corresponding antibodies.</p
Gene and cDNA structures of the novel splicing variant of mouse <i>Pparγ</i>.
<p>(A) Alignment of 5′-end sequences of <i>Pparγ1sv</i>, <i>Pparγ1</i>, and <i>Pparγ2</i> cDNAs. Each initiation codon is outlined, and exon 1, which is common to all three, is underlined. (B) Gene structure of N-terminal exons and common exon 1 of mouse <i>Pparγ</i> on chromosome 6. Distances between two exons and exon lengths are indicated as numbers of nucleotides. Arrows indicate the positions of the transcription initiation site of each transcription variant. (C) Multiple alignment of nucleotide sequences of mouse exon C and corresponding exons in other mammals. Distances between the 5′-end of each cDNA and exon C or corresponding exons of other mammals are indicated as numbers of base pairs.</p
Tissue distribution and relative abundance of three <i>Pparγ</i> transcripts.
<p>(A) Schematic representation of three mouse <i>Pparγ</i> cDNAs. The positions of unique forward primers for each transcript and common reverse primer binding sites for qPCR analyses are indicated as arrows. The size of each PCR product is indicated in parenthesis. (B) Expression levels of <i>Pparγ1sv</i>, <i>Pparγ1</i>, and <i>Pparγ2</i> transcripts in mouse tissues were evaluated by qPCR analysis using the normalized first strand cDNAs as a template. The values represent the mean with error bars of triplicate measurements. (C) Expression levels of <i>Pparγ1sv</i>, <i>Pparγ1</i>, and <i>Pparγ2</i> transcripts in mouse white adipose tissue and brown adipose tissue. The values are normalized to the amount of 18S ribosomal RNA. The column denotes the data mean obtained from tissues of four animals. *<i>P</i><0.01.</p