Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029463 (osteosarcoma)
 16,637 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Staphylococci are frequently isolated from human, animal and environmental samples. The genus Staphylococcus comprises 27 species, of which 23 are coagulase-negative. The pathogenic role of the coagulase-negative species remains to be fully established. Staphylococcus lugdunensis is a recently described coagulase-negative species. Its Latin name reflects the city (Lyon, France) where the bacteria was first described. The present study reports 7 cases of human infection caused by S. lugdunensis. Case 1: a 64 y/o diabetic woman in whom S. lugdunensis was isolated in the conjunctival exudate. Case 2: a 51 y/o male diagnosed of a bladder tumor, with S. lugdunensis detected in the purulent exudate of a transurethral resection. Case 3: an 81 y/o woman with cerebrovascular stroke, in whom S. lugdunensis was isolated from urine. Case 4: a 65 y/o male with bacterial endocarditis and S. lugdunensis isolation in blood culture. Case 5: a 79 y/o male with liver cirrhosis and S. lugdunensis in blood culture. Case 6: a 75 y/o female with cerebrovascular stroke, in whom S. lugdunensis was isolated from urine. Case 7: a 77 y/o male diagnosed of femoral osteosarcoma and isolation of S. lugdunensis in the purulent exudate of the wound. The present communication broadens the range of clinical syndromes in which coagulase-negative S. lugdunensis appears as pathogen.
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PMID:[7 cases of Staphylococcus lugdunensis infection]. 1048 38

A case of radiation-induced sarcoma of the chest wall is reported. Twenty-seven years 11 months after orthovoltage radiotherapy of the right breast a 69-year-old woman developed a radiation-induced osteosarcoma of the right thoracic wall. Initial diagnosis has been T-cell lymphoma of the skin. The right breast was irradiated with tangential fields and a total dose of 40 Gy, 2 Gy/day, 5 days a week. Orthovoltage treatment was performed in two courses of 20 Gy, 3 months apart. The clinical appearance of the secondary sarcoma was a diffuse infiltrated area in the irradiated breast which seemed to be fixed to the chest wall. Magnetic resonance imaging (MRI) demonstrated a mass in the right anterior thoracic wall which destroyed the fourth to the sixth rib. The tumor infiltrated the thoracic wall, including subcutaneous tissue and pericardium, as well as extending into the subphrenic space. Biopsy of the lesion revealed a poorly differentiated osteosarcoma. The patient's general condition precluded surgical or chemotherapeutic intervention; she died due to a cerebral stroke 6 months later. This case fulfilled all criteria for radiation-induced sarcoma, as there was a prior history of radiotherapy, latency period of several years, development of sarcoma within the irradiated field, and histologic confirmation of sarcoma.
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PMID:Radiation-induced osteosarcoma of the chest wall. 1219 65

Primary cardiac neoplasms are rare and occur less commonly than metastatic disease of the heart. In this overview, current published studies concerning malignant neoplasms of the heart are reviewed, together with some insights into their aetiology, diagnosis and management. We searched medline using the subject 'cardiac neoplasms'. We selected about 110 articles from between 1973 and 2006, of which 76 sources were used to complete the review. Sarcomas are the most common cardiac tumours and include myxosarcoma, liposarcoma, angiosarcoma, fibrosarcoma, leiomyosarcoma, osteosarcoma, synovial sarcoma, rhabdomyosarcoma, neurofibrosarcoma, malignant fibrous histiocytoma and undifferentiated sarcoma. The classic symptoms of cardiac tumours are intracardiac obstruction, signs of systemic embolisation, and systemic or constitutional symptoms. However, serious complications including stroke, myocardial infarction and even sudden death from arrhythmia may be the first signs of a tumour. Echocardiography and angiography are essential diagnostic tools for evaluating cardiac neoplasms. Computed tomography and magnetic resonance imaging studies have improved the diagnostic approach in recent decades. Successful treatment for benign cardiac tumours is usually achieved by surgical resection. Unfortunately, resection of the tumour is not always feasible. The prognosis after surgery is usually excellent in the case of benign tumours, but the prognosis of malignant tumours remains dismal. In conclusion, there are limited published data concerning cardiac neoplasms. Therefore, a high level of suspicion is required for early diagnosis. Surgery is the cornerstone of therapy. However, a multi-treatment approach, including chemotherapy, radiation as well as evolving approaches such as gene therapy, might provide a better palliative and curative result.
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PMID:Malignant tumours of the heart: a review of tumour type, diagnosis and therapy. 1769 68

MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) is commonly associated with the A3243G mitochondrial DNA (mtDNA) mutation encoding the transfer RNA of leucine (UUR) (tRNA (Leu(UUR))). The pathogenetic mechanisms of this mutation are not completely understood. Neuronal functions are particularly vulnerable to alterations in oxidative phosphorylation, which may affect the function of the neurotransmitter glutamate, leading to excitotoxicity. In order to investigate the possible effects of A3243G upon glutamate homeostasis, we assessed glutamate uptake in osteosarcoma-derived cytoplasmic hybrids (cybrids) expressing high levels of this mutation. High-affinity Na(+)-dependent glutamate uptake was assessed as radioactive [(3)H]-glutamate influx mediated by specific excitatory amino acid transporters (EAATs). The maximal rate (V(max)) of Na(+)-dependent glutamate uptake was significantly reduced in all the mutant clones. Although the defect did not relate to either the mutant load or magnitude of oxidative phosphorylation defect, we found an inverse relationship between A3243G mutation load and mitochondrial ATP synthesis, without any evidence of increased cellular or mitochondrial free radical production in these A3243G clones. These data suggest that a defect of glutamate transport in MELAS neurons may be due to decreased energy production and might be involved in mediating the pathogenic effects of the A3243G mtDNA mutation.
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PMID:MELAS mitochondrial DNA mutation A3243G reduces glutamate transport in cybrids cell lines. 1845 61

Pyruvate treatment was found to alleviate clinical symptoms of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome and is highly promising therapeutic. Using capillary electrophoresis time-of-flight mass spectrometry (CE-TOFMS), we measured time-changes of 161 intracellular and 85 medium metabolites to elucidate metabolic effects of pyruvate treatment on cybrid human 143B osteosarcoma cells harboring normal (2SA) and MELAS mutant (2SD) mitochondria. The results demonstrated dramatic and sustainable effects of pyruvate administration on the energy metabolism of 2SD cells, corroborating pyruvate as a metabolically rational treatment regimen for improving symptoms associated with MELAS and possibly other mitochondrial diseases.
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PMID:Metabolomic profiling rationalized pyruvate efficacy in cybrid cells harboring MELAS mitochondrial DNA mutations. 2288 39

Nitric oxide (NO) is a free radical and a signaling molecule in several pathways, produced by nitric oxide synthase (NOS) from the conversion of L-arginine to citrulline. Supplementation of L-arginine has been used to treat MELAS (mitochondrial encephalopathy with lactic acidosis and stroke like syndrome), a mitochondrial disease caused by the m.3243A>G mutation. Low levels of serum arginine and endothelium dysfunction have been reported in MELAS and this treatment may increase NO in endothelial cells and promote vasodilation, decreasing cerebral ischemia and strokes. Although clinical benefits have been reported, little is known about NO synthesis in MELAS. In this study we found that osteosarcoma derived cybrid cells with high levels of m.3243A>G had increased nitrite, an NO metabolite, and increased intracellular NO, demonstrated by an NO fluorescent probe (DAF-FM). Muscle vessels from patients with the same mutation had increased staining in NADPH diaphorase, suggestive of increased NOS. These results indicate increased production of NO in cells harboring the m.3243A>G, however no nitrated protein was detected by Western blotting. Further studies are necessary to clarify the exact mechanisms of L-arginine effect to determine the appropriate clinical use of this drug therapy.
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PMID:Nitric oxide synthesis is increased in cybrid cells with m.3243A>G mutation. 2326 69

Spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP) are frequently used as rat models not only of essential hypertension and stroke, but also of attention-deficit hyperactivity disorder (ADHD). Normotensive Wistar-Kyoto rats (WKY) are used as the control rats in these cases. An increasing number of studies has demonstrated the critical role of the central nervous system in the development and maintenance of hypertension. In a previous study, we analyzed the gene expression profiles in the adrenal glands of SHR. Thus, in this study, we analyzed gene expression profiles in the brains of SHR in order to identify the genes responsible for causing hypertension and stroke, as well as those involved in ADHD. Using genome-wide microarray technology, we examined the gene expression profiles in the brains of 3 rat strains (SHR, SHRSP and WKY) when the rats were 3 and 6 weeks of age, a period in which the rats are considered to be in a pre-hypertensive state. Gene expression profiles in the brain were compared between SHR and WKY, and between SHRSP and SHR. A total of 179 genes showing a >4- or <-4-fold change in expression were isolated, and candidate genes were selected using two different web tools: the first tool was the Database for Annotation, Visualization and Integrated Discovery (DAVID), which was used to search for significantly enriched genes, and categorized them using Gene Ontology (GO) terms, and the second was the network explorer of Ingenuity Pathway Analysis (IPA), which was used to search for interaction networks among SHR- and SHRSP-specific genes. The IPA of SHR-specific genes revealed that prostaglandin E receptor 4 (Ptger4) is one of the candidate genes responsible for causing hypertension in SHR, and that albumin (Alb) and chymase 1 (Cma1) are also responsible for causing hypertension in SHR in the presence of angiotensinogen (Agt). Similar analyses of SHRSP-specific genes revealed that the angiotensin II receptor-associated gene (Agtrap) interacts with the FBJ osteosarcoma oncogene (Fos), and with the angiotensin II receptor type-1b (Agtr1b). As Agtrap and Agtr1b not only participate in the 'uptake of norepinephrine' and 'blood pressure', but also in the 'behavior' of SHRSP at 6 weeks of age, our data demonstrate a close association between hypertension and ADHD.
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PMID:Analysis of genes causing hypertension and stroke in spontaneously hypertensive rats: gene expression profiles in the brain. 2445 43