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OBJECTIVES Recent studies in selected human tumors have demonstrated reduced expression of HRK with hypermethylation. Because no similar study has been performed specifically in prostatic lesions, we examined whether the methylation status of HRK is altered in prostate cancers. METHODS We chose to analyze the hypermethylation status of HRK, the expression of HRK protein and mRNA with 12q13.1 loss of heterozygosity (LOH) and with p53 mutation, and lesion apoptotic indices as determined by transferase-mediated digoxigenin-tagged 16-desoxy-uridine-triphosphate nick end-labeling (TUNEL) assays in 53 prostate cancers. RESULTS Twenty of the 53 prostate cancers (38%) demonstrated hypermethylation in either the promoter or in exon 1 and, more significantly, the loss of HRK expression observed in 14 cancers by immunohistochemistry (IHC) was associated with promoter methylation. In addition, high apoptotic indices in tumors were related to positive HRK expression. Prostate cancers demonstrating HRK methylation also showed methylation of multiple other genes, such as p14ARF, p16INK4a, O6-MGMT, and GTS-P, but, with the exception of one case, p53 mutations were not detected. When compared to tumors having a Gleason score (GS) of 5–6, a significant difference in the apoptotic indices was found among prostate cancers of GS 7 (P

A 47-year-old woman with previous history of transvaginal uterectomy 4 years before, presented to another hospital complaining of pollakisuria and pain during micturition. She was treated with antibiotics, but symptoms failed to resolve. So she referred to our department for investigations and treatments. On cystoscopy, there was a large mass with edematous mucosa in the anterior wall of bladder. Magnetic resonance image demonstrated an 8 cm irregularly-formed cystic mass which occupied dome of bladder. Resection of the mass including partial cystectomy was performed. This cystic mass contained retained 3 silk sutures surrounded by green color pus. Microscopic examination revealed inflammatory granulations without any malignancy. Because of the previous history, she was diagnosed as paravesical suture abscess due to infected silk materials at transvaginal uterectomy. Paravesical suture abscess is very rare complication of inguinal herniorrhaphy and mimics bladder or urachal neoplasm. In review of previously reported cases, the symotoms were predominantly urological. For avoiding unnecessary examinations and treatments, it is important to consider paravesical suture abscess in cases with histories of inguinal herniorrhaphy or other intra-pelvic operations. To our knowledge, there is no case report of paravesical abscess formation associated with transvaginal uterectomy and the present case is the first one for report.

In order to study multiple contiguous prostate cancer lesions, we constructed computer-assisted, three-dimensional models of multifocal prostate cancer specimens obtained by radical prostatectomy. We then examined the genetic heterogeneity among the specimens by DNA microarray analysis. Cancer foci with high Gleason patterns were found to occur de novo, whereas those with low Gleason patterns occurred contiguously with cancers of low Gleason patterns. Three-dimensional analysis showed that distinct, noncontiguous cancerous foci were genetically independent and multicentric. In contrast some contiguous multifocal lesions had the same genetic origin.

The present study was conducted to compare the incidences of renal tumors in Wistar (W), Fischer (F) and F1 rats (WF: female Wistar rats×male Fischer rats; FW: female Fischer rats×male Wistar rats) induced by N -ethyl- N -hydroxyethylnitrosamine (EHEN). Levels of 8-OHdG in renal DNA were also investigated in Wistar and Fischer rats. After 2000 ppm of EHEN was administered orally for 2 weeks, the animals were fed basal diet until week 32. Wistar males and females demonstrated significantly higher sensitivity regarding induction of renal lesions, while both WF and FW rats had similar incidences, generally intermediate between those for the two parent strains. The formation of 8-OHdG was maximal 60–180 min after an intraperitoneal dose of 750 mg/kg to Wistar and Fischer rats, which correlates with the increase tending to the incidence of renal tumors in male and female Wistar and Fischer rats. The results suggest that EHEN induction of renal tumors is related to oxygen radical damage and that the genes in the Wistar strain responsible for the sensitivity are not inherited in a sex-dependent fashion, despite the male being more susceptible.

3種類の市販C重油の水面上における重油の広がり状態について観察した。具体的には, 水面上における油膜面積の経時変化と温度, 流動点, 動粘度との関係を調べた。その結果, 油膜の広がりは重油の種類に依存し, ある温度以上で急激に広がることが見い出された。またこの温度は, 重油の動粘度と密接な関係があり, 本実験で用いた重油の場合, 動粘度が6000mm2/sになる温度と油膜が急激に広がる温度とが一致した。

Green tea consumed as a beverage in Asia contains polyphenols, which contain about a 15% mixture of catechins. The present paper reports the effect of polyphenon-60 (60% pure catechin) on the development of renal cell neoplasms in Wistar rats pretreated with N-ethyl-N-hydroxyethylnitrosamine (EHEN): 0.1% polyphenon-60 in block diet was given over a period of 30 weeks while EHEN was given in drinking water for 2 weeks. The results appears to show a tendency for green tea catechins (GTC) to decrease the incidence of renal cell tumors greater than 3 mm in diameter in Wistar rats but not tumors that are less than 3 mm in diameter. Polyphenon-60 did not affect EHEN initiation in the kidneys of rats. It is postulated that free radicals induced by EHEN may be suppressed by GTC, resulting in a lowering of the tendency for tumor growth.

We previously reported that treatment of Fischer-344 rats with 2-amino-4,5-diphenylthiazole (DPT) results in renal cystic changes. The present study was undertaken to examine the effects of long-term DPT treatment after initiation of kidney carcinogenesis with N-ethyl- N-hydroxyethylnitrosoamine (EHEN) in Wistar rats. One hundred forty-four 6-wk-old male Wistar rats were divided into 6 equal receiving groups: 1000 ppm EHEN or normal tap water for 2 wk followed by 1.06% DPT or basal diet for the subsequent 14 or 30 wk. Controls were maintained without treatment throughout. Subgroups of 6 animals from each group were sacrificed after 8, 16, 24, and 32 wk for histopathological assessment of lesion development in the kidneys and liver. Animals treated with DPT first developed cystic changes of the kidneys (primarily at the corticomedullary border) after 8 wk of treatment, and these changes progressed with time thereafter. In the groups in which DPT treatment was discontinued after 14 wk, cysts then gradually decreased in size. All tumors detected in the kidneys were histopathologically diagnosed as renal cell adenomas. The tumor multiplicity after 32 wk of treatment was significantly higher in Group I, receiving EHEN + DPT for 30 wk (6.33 ± 4.46), and Group III, receiving EHEN + DPT for 14 wk (3.83 ± 1.57), than in Group V, EHEN alone (1.00 ± 0.58) (p < 0.05). Renal cell tumors within cysts were only seen in Groups I and III. The general bromodeoxyuridine labeling indices for the kidneys at week 32 were significantly higher in Group I (55.94 ± 21.08 cells/mm2) and Group III (53.75 ± 12.38 cells/mm2) than in Group V (22.38 ± 6.98 cells/mm2) (p < 0.05). In conclusion, DPT caused cystic changes in rat kidneys, which, however, gradually decreased in size after the treatment was discontinued, suggesting a reversible nature. DPT clearly also promotes renal tumor development after EHEN initiation, and this effect persists, to a certain extent, even after the insult is removed.

Eighty-three kidneys from autopsy cases, all more than 60 years of age, were used in the present studies. Three millimeter-thick step slices from all kidneys were embedded in paraffin, and serial sections from all blocks used for the immunohistochemical demonstration of Leu M1 (leukocyte membrane antigen) and LTA (Lotus tetragonolobus agglutinin) in cells of proximal convoluted tubular origin, and PNA (peanut agglutinin) and EMA (epithelial membrane antigen) in cells of distal convoluted tubular origin. The ABC staining method was used in all cases. A total of 65 renal cell adenomas found in 31 of the 83 kidneys consisted of 40 papillary, 20 tubular and 5 solid type lesions. The sizes of these renal cell adenomas were from 0.6 to 5 mm in diameter and compression of neighboring tissues was characteristic. Papillary renal cell adenomas were positive in their cytoplasms for Leu M1 and LTA in 7 cases and at their cell membranes for PNA and EMA in 33 cases. The respective figures for tubular renal cell adenomas were 6 cases for Leu M1 and LTA and 14 cases for PNA and EMA. All solid renal cell adenomas were positive in their cytoplasms for PNA and EMA. The immunohistochemical results thus indicated 13 of 65 lesions to have a proximal convoluted tubular cell origin and 52 to be possibly derived from distal convoluted tubules or collecting ducts. A role for metaplasia, however, could not be ruled out.

Background We evaluated the clinical significance and prognostic value of histopathological features of bladder cancer, such as subepithelial growth patterns and tumor growth pattern at the invasion front. Methods In total, 130 patients newly diagnosed with non-muscle invasive bladder cancer and underwent transurethral resection between 1998 and 2009 were enrolled. Subepithelial growth patterns consisting of endophytic growth pattern (EGP) and von Brunn's nest involvement (VBNI) were investigated using hematoxylin and eosin-stained slides, and their frequency of occurrence, prognostic value, and correlation with other clinicopathological features was evaluated. Results EGP and VBNI were found in 40 (30.8%) and 5 (3.9%) of the 130 cases, respectively. Of the 26 pT1 tumors, the growth pattern at the invasion front was trabecular in 17 (65.4%) and infiltrative in 9 (34.6%). Although 8 (47.1%) of 17 trabecular tumors coexisted with EGP, no cases with infiltrative tumors had EGP (p = 0.023). VBNI correlated with high tumor grades (p = 0.006) and lymphovascular involvement (p = 0.026). The multivariate Cox proportional hazards analysis revealed that tumor diameter less than 3 cm (p = 0.04) and intravesical bacillus Calmette-Guérin therapy (p = 0.004) were independent favorable prognostic factors for recurrence-free survival, whereas tumor stage was an independent poor prognostic factor for disease progression (p = 0.006). Conclusions Subepithelial growth patterns were not a significant prognostic factor in this study. Additionally, no tumors with an infiltrative growth pattern coexisted with EGP, suggesting that determining the presence of EGP might be helpful for managing non-muscle invasive bladder cancers.

Heparan sulfate proteoglycan syndecan-1, CD138, is well known to be associated with cell proliferation, adhesion, and migration in various types of malignancies. In the present study, we focused on the role of syndecan-1 in human urothelial carcinoma of the urinary bladder. Silencing of syndecan-1 by siRNA transfection down-regulated transcriptional factor junB and the long isoform of FLICE-inhibitory protein (FLIP long), resulting in the induction of apoptosis in the urothelial carcinoma cell lines UMUC2 and UMUC3. Knockdown of junB and FLIP long as well as syndecan-1 silencing mediated apoptosis that was inhibited by pan-caspase inhibitors. Transurethral injection of syndecan-1 siRNA into the urinary bladder significantly reduced syndecan-1 gene expression and growth of red fluorescent-labeled KU-7/RFP bladder cancer cells in the mouse orthotopic bladder cancer model. Immunohistochemical examination showed high syndecan-1 protein expression in high-grade, superficial, and deep invasive carcinomas (pT1 and >or=pT2) as well as carcinoma in situ, but not in low-grade and noninvasive phenotypes (pTa). In addition, the percentage of cancer cells positive for syndecan-1 at initial diagnosis was statistically associated with the frequency of bladder cancer recurrence after transurethral resection. In conclusion, syndecan-1 might contribute to urothelial carcinoma cell survival and progression; therefore, this molecule could be a new therapeutic target in human urinary bladder cancer.

Background The recent sport promotion and healthy boom brought increasing the sport population. Running especially is the most popular activity. Various urinary abnormalities are induced by strenunous exercise. Hematuria has been found after various sports activities and noted as sports hematuria by some studies. We evaluated relation between hematuria and running as the most popular sport in summer. Material and methods Urine samples were obtained from 109 healthy volunteers participated in 5 km run, at rest before and immediately after running. We could evaluate 90 of all and investigate counts and morphpology of urinary red cells by microscopic finding of urine sediments and analysis of flowcytometry for urinary cells. Results Eighty-three subjects had increased counts of urinary red cells after running. Of these, 32 had counts above the normal range, microscopic hematuria (RBC above 3/hpf). In analysis of these 32 had dysmorphic pattern mostly. Conclusion This study confirms that exercise induces hematuria easily and sports hematuria has a glomerular source chiefly.

家兎 (雄) に対しスミチオン [O, O-ジメチルO-(3-メチル-4-ニトロフェニル) ホスホロチオエート] を10および3mg/kg/dayの割合で飼料中に混ぜ6ヵ月間摂食させて, コリンエステラーゼ活性の変動と生体の機能および組織の構造とくに神経筋接合部に及ぼす影響との関係を検討した. 血漿, 血球コリンエステラーゼはいずれの投与群においても, 脳コリンエステラーゼは高濃度群において有意に阻害されていた. これに対し外眼筋コリンエステラーゼには生化学的にも組織化学的にも顕著な変化は認められず, 外眼筋の神経筋接合部の微細構造は電顕的には正常であった. また動物の挙動, 死亡率, 血液検査, 臨床生化学検査, 臓器重量, 病理組織学的検査においても異常は見いだされなかった. したがって, コリンエステラーゼ阻害を有機リン化合物による中毒症状に対する最も鋭敏な指標と考えてよいと思われる.

臨床肝血管腫3例と犬肝血管腫27病巣に肝血管造影,肝シンチグラムおよび血液生化学的検査を行い,その診断方法について検討した.血管造影で動脈相での栄養血管の拡張,血管性に富んだ異常血管群の出現,動脈相初期より静脈相にかけて明瞭にみられる斑状陰影により,臨床的に1.5×1.5cm大の血管腫を診断することが出来,小さな肝細胞癌との鑑別も可能であっだ.大きな血管腫では肝動脈枝の腫瘍による圧排,変位がみられ,腫瘍内に多数の新生血管やA-V shuntsが認められ,大きな肝細胞癌との鑑別が困難であった.犬肝血管腫では0.4×0.5cm大のものまで診断可能であり,直接3倍拡大撮影法を用いると0.4×0.3cm大の血管腫の質的診断まで可能となった.肝シンチグラムや血液生化学的検査は診断的価値はなかった.以上の事から肝血管造影が血管腫の診断に最も有用である結果が得られた.また肝血管腫の治療方針について自験例に文献的考察を加えて検討した.

Six groups of female outbred Wistar rats were subjected to the following treatments: 2,500 ppm 3-amino-1H-1,2,4-triazole (amitrole) administered in the drinking water (group I); partial thyroidectomy and administration of amitrole in the drinking water (group II); partial thyroidectomy plus autoimplantation of resected thyroid tissue plus administration of amitrole in the drinking water (group III); no treatment (control of group I) (group IV); partial thyroidectomy without amitrole administration (control of group II) (group V); or partial thyroidectomy plus autoimplantation of resected thyroid tissue without amitrole administration (control of group III) (group VI). Goiters developed in all rats given amitrole (groups I-III). Invasive growth of the proliferating follicular tissue through the capsule into adjacent fatty tissue and of pericapsular blood vessels was frequent in these groups (P less than 0.001); invasive lesions were more frequent in the lobectomized thyroid glands of rats (groups II and III). Seven papillary adenomas composed of atypical cells with hyperchromatic nuclei and many mitoses were found in the thyroid glands and grafts in amitrole-treated groups I-II. No invasive growth or adenomas appeared in the control rats of groups IV-VI. Cholangiofibrosis developed in 5 of 100 rats in groups I-III.