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A case of mucinous cystadenoma of the testis in a 55-year-old man is reported. The tumor was confined to the testis and was clearly separated from the epididymis. There was no connection between the tumor cyst and the rete testis. The lumen of the cyst was lined with a single-layer of columnar cells interspersed with goblet cells. There was neither stromal invasion nor metastasis to other organs and there were no ovarian or germ cell neoplastic elements in the tumor. Immunohistochemical analysis revealed that MUC2, MUC5AC, carcinoembryonic antigen, CA19-9, CK7 and CK20 proteins were expressed on the tumor epithelial cells, whereas expression of MUC6, α-fetoprotein, CA125, human chorionic gonadotrophin, estrogen receptor, progesterone receptor, calretinin, chromogranin A, p53, cyclin D1 and bcl-2 proteins was absent. Ki-67 protein was weakly and sparsely expressed in the nuclei of epithelial cells. The mucinous cystadenoma in the present case, which was devoid of a connection to testicular appendices and had the immunohistochemical characteristics of gastrointestinal mucosa, might have originated from one-sided differentiation of teratoma cells. [ABSTRACT FROM AUTHOR]

Ets-1 is a transcription factor regulating the expression of matrix-degrading proteinases and is believed to play a critical role in cell migration and tumor invasion. The aim of this study is to investigate the direct induction of ets-1 with consequential upregulation of collagenase-1 (MMP-1) by cell adhesion to extracellular matrix and to identify intracellular signal transduction pathways involved in ets-1 induction in cultured endothelial cells. The expressions of ets-1 mRNA and protein as well as MMP-1 protein were induced by cell adhesion to type I collagen and antisense ets-1 oligonucleotides impaired that MMP-1 expression. In addition, protein tyrosine kinase (PTK) and protein kinase C (PKC) inhibitors abrogated their induction, showing the suppression of focal adhesion kinase phosphorylation. These results suggest that ets-1 induced by cell adhesion to extracellular matrix directly upregulates MMP-1 expression via PTK and PKC activation in cultured endothelial cells. [Copyright &y& Elsevier]

Presents information on a study on the effect Ets-1 has on smooth muscle fiber. Identification of what Ets-1 is; Results of the study; Indication of how the study was conducted; What procedures were followed; Information on the substances used in the experiment.

Examines the stimulation of ets-1, a transcription factor by endothelin-1 (ET-1) and platelet-derived growth factor-BB (PDGF-BB) in vascular smooth muscle cells of rats. Dose-dependent expression of ets-1 messenger RNA; Significance of ets-1 in the orchestration of matrix proteinase expression and of vascular remodeling after arterial injury.

The active stage of ulcerative colitis (UC) involves transmigration of polymorphonuclear (PMN) cells to colonic epithelia. The angiopoietin (Ang) pathway plays a role as the regulator of PMN transmigration. To clarify the role of the Ang/Tie pathway in the activation of UC, especially in cypt abscess formation, 67 tissue samples were obtained from patients with UC and ten controls without UC for immunohistochemical analysis for the expression of Ang-1, -2, or Tie-2. The epithelia of crypt abscess was strongly positive for Ang-1 and -2 for all 57 samples derived from patients with active UC, though the colorectal epithelium without crypt abscess showed minimal expression of Ang-1, -2, and Tie-2. Numerous transepithelial migrating PMN cells in crypt abscesses also expressed Tie-2. The specimens of UC patients in remission showed significantly less immunoreactivity for Ang-1, -2, or Tie-2. These findings suggest that the Ang/Tie pathway may play a role in the progression of UC. [ABSTRACT FROM AUTHOR]

Norepinephrine is considered to possess potent anti-apoptotic action in regenerating hepatocytes. To clarify the role of the sympathetic nervous system in apoptosis that occurs in chronic liver damage and following the promotion of liver cirrhosis, we studied a carbon tetrachloride (CCl4)-induced liver injury model, using spontaneously hypertensive rats (SHR), Wistar-Kyoto rats (WKY), and chemically sympathectomized WKY. At 24 h after CCl4 administration. acute damage, characterized by vacuolated hepatocytes in the centrilobular zone, was greater in SHR than in WKY. This vacuolated change in WKY hepatocytes was significantly reduced by chemical sympathectomy with 6-hydroxydopamine (6-OHDA). After 48 h, the acute damage was dramatically improved in each animal, without significant differences between the three groups. In chronic damage after weekly repetition of CCl4 treatment for 4 weeks, fibrosis was evident in SHR, while in the other groups there was only scant fibrosis in the centrilobular zone. After 8 weeks' repetition of CCl4, liver cirrhosis was seen only in SHR. The incidence of apoptotic cells in areas of both acute and chronic damage in WKY, detected by terminal deoxynucleotidyl transferase-dUTP nick end labeling, was significantly increased in comparison with that in SHR, and was further increased by 6-OHDA pretreatment. In contrast, there was significantly greater enhancement of the growth of hepatocytes in SHR than in WKY in both acute and chronic damage. Moreover. hepatocyte growth kinetics in WKY was significantly inhibited after sympathectomy in acute injury, as evidenced by immunohistochemistry for proliferating cell nuclear antigen (PCNA). In vitro, the amount of hepatocellular apoptosis induced by transforming growth factor-beta1 was significantly decreased by incubation with norepinephrine. These findings suggest that the anti-apoptotic effect of the sympathetic nervous system increases cell growth kinetics and promotes liver cirrhosis in this animal model. [ABSTRACT FROM AUTHOR]

Oxygen (O2) is a prerequisite for cellular respiration in aerobic organisms but also elicits toxicity. To understand how animals cope with the ambivalent physiological nature of O2, it is critical to elucidate the molecular mechanisms responsible for O2 sensing. Here our systematic evaluation of transient receptor potential (TRP) cation channels using reactive disulfides with different redox potentials reveals the capability of TRPA1 to sense O2. O2 sensing is based upon disparate processes: whereas prolyl hydroxylases (PHDs) exert O2-dependent inhibition on TRPA1 activity in normoxia, direct O2 action overrides the inhibition via the prominent sensitivity of TRPA1 to cysteine-mediated oxidation in hyperoxia. Unexpectedly, TRPA1 is activated through relief from the same PHD-mediated inhibition in hypoxia. In mice, disruption of the Trpa1 gene abolishes hyperoxia- and hypoxia-induced cationic currents in vagal and sensory neurons and thereby impedes enhancement of in vivo vagal discharges induced by hyperoxia and hypoxia. The results suggest a new O2-sensing mechanism mediated by TRPA1. [ABSTRACT FROM AUTHOR]

Serratia marcescens is an ubiquitous, saprophytic gram-negative bacillus that is associated with infections such as bacteremia, pneumonia and osteomyelitis. However, it has not been known to form granulomas. A 72-year-old man with a history of tricuspidal insufficiency, mitral insufficiency and ureterolithiasis presented with lumbago on the left side. He was admitted to our hospital, where abscess formation in the subcapsular space and perirenal fat space of the left kidney, and left renal calculi were identified by computed tomography of the abdomen. As infection and/or a tumor were suspected, nephrectomy was performed. The histopathological findings in the resected kidney indicated severe infiltration by inflammatory cells with lymphoid follicles in the interstitium, and the proliferation of mesangial cells and matrix in glomerulus. Furthermore, giant cell granulomas were observed in the soft tissue around the kidney. As an aerobic culture of the abscess from the granulomas only produced Serratia marcescens, these granulomas were diagnosed as Serratia marcescens granulomas. In addition, expressions of PTHrP and PTH/PTHrP-receptor were observed in the giant cells in Serratia granuloma, which suggested that PTHrP might be involved in giant cell formation in Serratia granuloma by autocrine and/or paracrine mechanisms. [ABSTRACT FROM AUTHOR]

The aim of this study was to examine whether transcription factor ETS-1, which is responsible for the expression of metalloproteinases and integrin β3, is implicated in the induction of nitric oxide (NO)-induced angiogenesis. Bovine aortic endothelial cells were cultured on type I collagen gel to measure the length of the formed tube-like structure, which is a marker for in vitro angiogenesis. The addition of S-nitroso-N-acetylpenicillamine (SNAP), an NO-donor, to confluent endothelial cells stimulated the formation of the tube-like structure, with disappearance of covered endothelial cell monolayers. Another NO-donor 2,2′-(hydroxynitrosohydrazono)bis-ethanamine (NOC 18) also induced the formation of the tube-like structure. In contrast to the induction of the formation of the tube-like structure by SNAP, it reduced cell proliferation. SNAP and NOC 18 also increased the expression of the ets-1 mRNA level in a concentration-dependent manner. The maximum expression was observed at 2 h after their addition. Moreover, the SNAP-induced in vitro angiogenesis, ets-1 mRNA expression and ETS-1 protein expression were strongly reduced by the treatment with ets-1 antisense oligonucleotide. These results strongly suggest that NO stimulates in vitro angiogenesis through the induction of ETS-1 expression. NO appears to stimulate endothelial cell differentiation to the angiogenic phenotype via the induction of ETS-1 transcription factor. [Copyright &y& Elsevier]

Studies the differential roles of intercellular adhesion molecule -1 and E-selection in polymorphonuclear leukocyte-induced angiogenesis. Role of metalooproteinase gene transcription in angiogenesis; Enhancement of the activated polymorphonuclear leukocytes (PMN) in the angiogenesis; Addition of activated PMN to endothelial cells.