Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Major ablative hepatic resection is often indicated in children with solid liver tumors, and reduction of operative blood transfusion is a primary goal. Total hepatic occlusion (THO) is an effective method that is well established in adults, yet its role in children is less well described. We describe our preliminary experience with THO in children assessing surgical outcome. The charts of seven children (ages 5 months to 7 years, weight 6-30 kg) who underwent THO during hepatectomy (four right and three left lobectomies) for liver tumors (hepatoblastoma in three, metastatic Wilm's tumor in two, mesenchymal hamartoma in one, and angiosarcoma in one) between January 1997 and June 2002 were reviewed. THO was established in all cases by clamping the supra- and infrahepatic inferior vena cava and the porta hepatis. Surgical parameters assessed included: 1) warm ischemia time, 2) operative blood transfusion, 3) operative complications, and 4) tumor resection margins. THO was successful in six of the seven cases (85.7%). In one case systemic hypotension unresponsive to fluid resuscitation developed at the outset with THO requiring conversion to pedicle clamping to perform the hepatectomy. Mean warm ischemia time during THO was 26 minutes (range 18-45 minutes). Mean estimated blood loss was 221 cm3 (range 50-800 cm3). Operative blood transfusion was required in one of six patients (15 cm3/kg). Excluding the "failed" THO case (intraoperative hypotension) there were no significant intraoperative or postoperative complications. All seven children had curative resections as indicated by "tumor-free" microscopic margins. We conclude that total hepatic occlusion can be performed safely and successfully for pediatric liver tumors. Operative blood transfusion appears to be minimized.
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PMID:Hepatectomy in children under total hepatic occlusion. 1285 17

An 85-yr-old male presented with complaints of a 40-lb weight loss and a dull left upper quadrant abdominal pain. He also complained of decreased appetite, generalized weakness, generally not feeling well, and a dull left upper quadrant abdominal pain that was not relieved by food. He had a ventral and a left-sided inguinal hernia. Laboratory investigations revealed iron deficiency anemia, the cause of which was not apparent despite extensive investigation including computerized tomographic scans, esophagogastroduodenoscopy, and small-bowel follow-through examination. Surgical exploration for possible angiodysplasia, malignancy, and/or mesenteric ischemia revealed an incarcerated hernia, and the histopathological examination of the surgical specimen revealed high-grade angiosarcoma. The tumor showed strong positivity for vimentin and CD31 and a focal positivity for Factor VIII and CD34. At that time he was found to have hepatic metastases. He was started on thalidomide as an experimental measure with no change in the performance status and increasing evidence of necrosis in the metastatic lesion.
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PMID:Angiosarcoma of the small intestine: a possible role for thalidomide? 1471 38

Aortic angiosarcomas, one of the three major types of primary aortic tumors, are exceedingly rare, with only 25 cases reported in the literature. Peripheral thromboembolic complications are the most frequently described presenting feature, and therefore, these tumors can be mistaken for aortoiliac occlusive disease. We describe a rare case of an extensive thoracoabdominal angiosarcoma that manifested with hypertension, profound anemia, and visceral ischemia in a young woman.
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PMID:Angiosarcoma of the thoracoabdominal aorta presenting with systemic hypertension, anemia, and visceral ischemia. 1836 72

Nestin is a class VI intermediate filament protein expressed in the cytoplasm of stem and progenitor cells in the mammalian CNS during development. In adults, nestin is present only in a small subset of cells and tissues, including the subventricular zone of the adult mammalian brain, where neurogenesis occurs. Nestin expression has also been detected under such pathological conditions as ischemia, inflammation, and brain injury, as well as in various types of human solid tumors and their corresponding cell lines. Furthermore, nestin was recently found in the nuclei of glioblastoma, neuroblastoma, and angiosarcoma cells and it was proved to interact directly with the nuclear DNA in neuroblastoma cells. Here, we perform the first study of the intracellular distribution of nestin in cell lines derived from neurogenic tumors. Using immunodetection methods, we examined nestin expression in tumor-derived cell lines obtained from 11 patients with neuroblastoma, medulloblastoma, or glioblastoma multiforme. Besides its standard cytoplasmic localization, nestin was present in the nuclei of two neuroblastoma cell lines and one medulloblastoma cell line. Nestin was only present in the nuclei of cells with diffuse cytoplasmic staining for this protein, and the proportion of cells positive for nestin in nuclei, as well as the intensity of staining, varied. The presence of nestin in the nuclei was confirmed by both transmission electron microscopy and Western blotting. Our results indicate that the presence of nestin in the nuclei of tumor cells is not very rare, especially under in vitro conditions.
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PMID:Analysis of nuclear nestin localization in cell lines derived from neurogenic tumors. 2134 Apr 83

Neovascularization in cancer or retinopathy is driven by pathological changes that foster abnormal sprouting of endothelial cells. Mouse genetic studies indicate that the stress-induced small GTPase RhoB is dispensable for normal physiology but required for pathogenic angiogenesis. In diabetic retinopathy, retinopathy of prematurity (ROP) or age-related wet macular degeneration (AMD), progressive pathologic anatomic changes and ischemia foster neovascularization are characterized by abnormal sprouting of endothelial cells. This process is driven by the angiogenic growth factor VEGF, which induces and supports the formation of new blood vessels. While injectable biologics targeting VEGF have been used to treat these pathological conditions, many patients respond poorly, prompting interest in other types of mechanism-based therapy. Here we report the preclinical efficacy of a monoclonal antibody that specifically targets RhoB, a signaling molecule that is genetically dispensable for normal physiology but required for pathogenic retinal angiogenesis. In murine models of proliferative retinal angiogenesis or oxygen-induced retinopathy, administering a monoclonal RhoB antibody (7F7) was sufficient to block neoangiogenesis or avascular pathology, respectively. Our findings offer preclinical proof of concept for antibody targeting of RhoB to limit diabetic retinopathy, ROP or wet AMD and perhaps other diseases of neovasculogenesis such as hemangioma or hemangiosarcoma nonresponsive to existing therapies.
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PMID:RhoB antibody alters retinal vascularization in models of murine retinopathy. 3053 63