Hemorrhagic Necrosis (hemorrhagic + necrosis)

Distribution by Scientific Domains


Selected Abstracts


Phase-contrast X-ray imaging with a large monolithic X-ray interferometer

JOURNAL OF SYNCHROTRON RADIATION, Issue 4 2000
Tohoru Takeda
To increase the field of view for large objects in phase-contrast X-ray imaging, a large monolithic X-ray interferometer has been fabricated using an available silicon ingot of diameter 10,cm. A performance study of this interferometer has been carried out using a synchrotron X-ray source. The view size of the interference pattern obtained with this interferometer was 25,mm wide and 15,mm high and its visibility was 79%. Various structures of a sliced human hepatocellular carcinoma were identified as necrosis, hemorrhagic necrosis, normal liver tissue and blood vessel. The performance of this interferometer was sufficient for phase-contrast X-ray imaging. [source]


A20 protects mice from lethal liver ischemia/reperfusion injury by increasing peroxisome proliferator-activated receptor-, expression

LIVER TRANSPLANTATION, Issue 11 2009
Haley E. Ramsey
The nuclear factor-,B inhibitory protein A20 demonstrates hepatoprotective abilities through combined antiapoptotic, anti-inflammatory, and pro-proliferative functions. Accordingly, overexpression of A20 in the liver protects mice from toxic hepatitis and lethal radical hepatectomy, whereas A20 knockout mice die prematurely from unfettered liver inflammation. The effect of A20 on oxidative liver damage, as seen in ischemia/reperfusion injury (IRI), is unknown. In this work, we evaluated the effects of A20 upon IRI using a mouse model of total hepatic ischemia. Hepatic overexpression of A20 was achieved by recombinant adenovirus (rAd.)-mediated gene transfer. Although only 10%-25% of control mice injected with saline or the control rAd., galactosidase survived IRI, the survival rate reached 67% in mice treated with rAd.A20. This significant survival advantage in rAd.A20-treated mice was associated with improved liver function, pathology, and repair potential. A20-treated mice had significantly lower bilirubin and aminotransferase levels, decreased hemorrhagic necrosis and steatosis, and increased hepatocyte proliferation. A20 protected against liver IRI by increasing hepatic expression of peroxisome proliferator-activated receptor alpha (PPAR,), a regulator of lipid homeostasis and of oxidative damage. A20-mediated protection of hepatocytes from hypoxia/reoxygenation and H2O2 -mediated necrosis was reverted by pretreatment with the PPAR, inhibitor MK886. In conclusion, we demonstrate that PPAR, is a novel target for A20 in hepatocytes, underscoring its novel protective effect against oxidative necrosis. By combining hepatocyte protection from necrosis and promotion of proliferation, A20-based therapies are well-poised to protect livers from IRI, especially in the context of small-for-size and steatotic liver grafts. Liver Transpl 15:1613,1621, 2009. © 2009 AASLD. [source]


Segmental testicular infarction due to cholesterol embolism: Not the first case, but the first report

PATHOLOGY INTERNATIONAL, Issue 11 2008
Shiro Adachi
Segmental infarction of the testis represents a rare entity in that there have been fewer than 40 cases documented in the literature. Like global infarction, segmental infarction of the testis can masquerade as a mass lesion or torsion of the testis. Reported herein is a very rare case of segmental testicular infarction due to atheroembolism in a 58-year-old man. The patient presented with severe left testicular pain and underwent left high orchiectomy on the clinical diagnosis of testicular torsion. The testis had a segmental hemorrhagic necrosis around which many cholesterol emboli were observed. This is the first report to describe cholesterol embolism-associated segmental testicular infarction. [source]


Low-grade renal cell carcinoma arising from the lower nephron: A case report with immunohistochemical, histochemical and ultrastructural studies

PATHOLOGY INTERNATIONAL, Issue 12 2001
Masako Otani
Most renal cell carcinomas (RCC) are composed of clear cells with sinusoid-like vasculatures and originate from the proximal tubule. On the other hand, collecting duct carcinoma (CDC) and chromophobe RCC are thought to originate from the lower nephron. In the present study, we present a case of unusual RCC. The patient was a 68-year-old Japanese woman who had developed general fatigue with hematuria. Computed tomography revealed a left renal tumor suggesting sarcoma. The resected tumor was located in the renal parenchyma, measuring 12 × 10 × 8 cm in size. Histologically, the tumor consisted principally of cuboidal cells forming parallel or radiating arrays, continuous with the spindle-shaped cells. Most parts of the tumor showed hemorrhagic necrosis. Immunohistochemically, tumor cells were positive for high molecular weight cytokeratins, vinculin, vimentin, CD15 and epithelial membrane antigen, and showed affinities with some kinds of lectins. N- and E-cadherins and , -catenin were diffusely positive in tumor cells. Nuclear positivity for Ki-67 and p53 protein were approximately 2.0 and 1.7%, respectively. Considering its morphological and histochemical natures, this tumor is considered to have originated from the lower nephron, which is unique for a tumor of low-grade malignancy. [source]


Downregulation of Tie2 gene by a novel antitumor sulfolipid, 3,-sulfoquinovosyl-1,-monoacylglycerol, targeting angiogenesis

CANCER SCIENCE, Issue 5 2008
Yoko Mori
We previously reported that 3,-sulfoquinovosyl-1,-monoacylglycerol (SQMG) was effective in suppressing the growth of solid tumors due to hemorrhagic necrosis in vivo. In the present study, we investigated the antiangiogenic effect of SQMG. In vivo assessment of antitumor assays showed that some tumor cell lines, but not others, were sensitive to SQMG. Microscopic study suggested that in SQMG-sensitive tumors, but not SQMG-resistant tumors, angiogenesis was reduced. We next investigated gene expression relating to angiogenesis in tumor tissues by quantitative real-time polymerase chain reaction. Consequently, although vascular endothelial growth factor gene expression was not detected with significant differences among the cases, significant downregulation of Tie2 gene expression was observed in all SQMG-sensitive tumors as compared with controls, but not in SQMG-resistant tumors. These data suggested that the antitumor effects of SQMG could be attributed to antiangiogenic effects, possibly via the downregulation of Tie2 gene expression in SQMG-sensitive tumors. (Cancer Sci 2008; 99: 1063,1070) [source]