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Biomedical subjects

J Rössler

Publications and source records attributed to J Rössler.

At least 19 recordsLinked to original sources
PubMed2004

Parkes Weber or Klippel-Trenaunay syndrome? Non-invasive diagnosis with MR projection angiography.

Klippel-Trenaunay and Parkes Weber (Klippel-Trenaunay-Weber) syndromes consist of vascular malformations of the capillary, venous and lymphatic systems combined with soft tissue and bone hypertrophy of the affected extremity. Klippel-Trenaunay syndrome is a pure low-flow condition, while Parkes Weber syndrome is characterized by significant arteriovenous fistulas. The distinction of both entities is relevant, since the prognosis and therapeutic strategies differ significantly. Our purpose is to demonstrate that thick-slice dynamic magnetic resonance projection angiography (MRPA) is a non-invasive tool to detect arteriovenous shunting in Parkes Weber syndrome. Four patients underwent MR imaging and MRPA. MRPA demonstrated arteriovenous shunting in three patients. Arteriovenous shunting was characterized by early appearing draining veins. The time of arrival between normal arteries and pathological veins varied between less than 0.5 and 1.0 s. Therefore, the diagnosis in these cases could be specified as Parkes Weber syndrome. In all these cases, arteriovenous shunting was confirmed by intraarterial digital subtraction angiography. One patient showed normal results in MRPA and could be diagnosed as having Klippel-Trenaunay syndrome.

Adult↗
PubMed2003

Head and neck vascular malformations: time-resolved MR projection angiography.

Extracranial vascular anomalies can be divided into haemangiomas and vascular malformations. The latter can be subdivided on the basis of the predominant type of vascular channels. Separation of high- and low-flow vascular malformations is of clinical importance. We report preliminary observations on time-resolved magnetic resonance projection angiography (MRPA) of vascular malformations of the head and neck. We examined eight patients with vascular anomalies of the head and neck. On MRPA the time between the early arterial phase and enhancement of the malformation could be used to distinguish high- and low-flow lesions. High-flow arteriovenous malformations showed early, intense enhancement. Venous malformations were either not visible on MRPA or showed late enhancement of veins. One patient was examined after embolisation of an arteriovenous fistula of the mandible. Normal MRPA was taken to indicate absence of a residual lesion.

Adolescent↗
PubMed2001

Quantification of angiogenesis stimulators in children with solid malignancies.

Humoral angiogenesis stimulators including vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) have been implicated in the pathogenesis of solid malignancies. However, it has remained unclear whether both stimulators contribute to the development and progression of solid malignancies of children. The aim of the present study was to determine whether VEGF and bFGF are elevated in body fluids of children with solid malignancies and, if so, whether these elevated levels correlate with clinical parameters. Using enzyme-linked immunosorbent assays (ELISAs), we quantified VEGF and bFGF in serum (n = 107) and urine (n = 57) of healthy children and of children with solid malignancies (serum: n(VEGF) = 69, n(bFGF) = 60; urine: n(VEGF) or n(bFGF) = 13). Finally, we compared patients' pre-therapeutic and post-therapeutic levels. Serum VEGF was elevated in children with several solid tumors (Ewing's sarcoma, primitive neuroectodermal tumours, malignant lymphoma, Langerhans cell histiocytosis and medulloblastoma). In contrast, serum bFGF, urinary bFGF or urinary VEGF were not significantly elevated. Upon successful therapy, elevated pre-therapeutic serum VEGF levels declined to levels present in healthy children. VEGF could contribute to the progression of pediatric solid malignancies, and serum VEGF could be used to monitor therapeutic response. Furthermore, the determination of angiogenesis stimulators could identify patients eligible for anti-angiogenic therapy.

Adolescent↗
PubMed2001

Hypoxia promotes apoptosis of human neuroblastoma cell lines with enhanced N-myc expression.

We have examined the effect of hypoxia and nutrient depletion on the growth of human neuroblastoma cells with normal or enhanced expression of the N-myc oncogene. The combination of both conditions reduced the growth of neuroblastoma cells with normal N-myc expression. However, this effect was much more pronounced in neuroblastoma cells with enhanced N-myc expression and eventually resulted in apoptosis, presumably by the up-regulation of CD95. Our data suggest that therapeutic induction of tumor hypoxia and nutrient depletion (for example, by anti-angiogenesis) could help to improve the outcome of patients with neuroblastomas carrying the prognostically unfavourable N-myc amplification.

Apoptosis↗
PubMed2001

Primary B-cell lymphoma of bone in children.

UNLABELLED: Primary lymphoma of bone (PLB) is a rare entity of extranodal non-Hodgkin lymphoma (NHL). We report on two children with PLB focussing on diagnostic evaluation and treatment strategy. Clinical and radiographic presentation in both children suggested a primary bone tumour such as Ewing sarcoma. A 13-year-old girl showed osteolytic tumours in the right 7th rib and right iliac crest. Additional skeletal lesions were found by whole-body positron emission tomography. A 6-year-old boy presented with an isolated, osteolytic lesion of the left distal femur. In both patients staging procedures excluded any organ involvement besides the skeletal tumours. Tumour biopsy and immunohistological studies revealed lymphoblastic non-Hodgkin lymphoma of B-cell lineage in both children. They received a polychemotherapy for B-cell lymphoma according to the NHL-BFM 95 protocol and are in complete remission with a follow up of 24 and 18 months respectively. CONCLUSION: Isolated, primary lymphoma of bone in children may clinically and radiographically impose as primary bone tumour. Multiple therapeutic strategies have been applied in the treatment of this malignancy, however, treatment modalities are not well focussed on immunological patterns in the case of primary lymphoma of bone. Staging techniques should include immunophenotyping to initiate specific cell lineage treatment.

Adolescent↗
PubMed2000

The N-myc oncogene in human neuroblastoma cells: down-regulation of an angiogenesis inhibitor identified as activin A.

Angiogenesis, the formation of new blood vessels, is seen during embryonic development and tumor progression, but the mechanisms have remained unclear. Recent data indicate that developmental and tumor angiogenesis can be induced by cellular oncogenes, leading to the enhanced activity of molecules stimulating angiogenesis. However, activated oncogenes might also facilitate angiogenesis by down-regulating endogenous inhibitors of angiogenesis. We report here that enhanced expression of the N-myc oncogene in human neuroblastoma cells down-regulates an inhibitor of endothelial cell proliferation, identified by amino acid sequencing as being identical with activin A, a developmentally regulated protein. Down-regulation appears to involve interaction of the N-Myc protein with the activin A promoter. In addition, activin A inhibits both endothelial cell proliferation in vitro and angiogenesis in vivo, and it induces hemorrhage in vivo. We suggest that the N-myc-induced down-regulation of activin A could contribute to developmental and tumor angiogenesis.

Activins↗
PubMed2000

N-myc down-regulates activin A.

N-myc oncogene amplification is frequent in human neuroblastoma and predicts poor prognosis, but the molecular consequences have remained obscure. We report here that enhanced N-myc expression correlates with low or undetectable expression of activin A, but not other closely related members of the transforming growth factor-beta superfamily. N-myc interacts with the activin A promoter, eventually inducing down-regulation of activin A mRNA and protein. This study demonstrates for the first time N-myc-induced down-regulation of a gene implicated in signal transduction. Down-regulation of activin A could deprive neuroblastomas from a signal with growth-inhibitory activities toward the tumor and its stroma and thereby permit neuroblastoma progression.

Activins↗
PubMed1999

Arginine deiminase inhibits cell proliferation by arresting cell cycle and inducing apoptosis.

We have previously demonstrated that arginine deiminase inhibits the proliferation of vascular endothelial cells, but the mechanisms leading to growth inhibition have remained unclear. We report here that low concentrations of arginine deiminase purified from Mycoplasma arginini inhibit proliferation of various cultured cells by arresting the cell cycle in G(1) and/or S phase with higher arginine deiminase concentrations leading to subsequent apoptosis. Our results demonstrate that arginine deiminase inhibits cell proliferation not only by depletion of arginine, but also by mechanisms involving the cell cycle and death signals.

Apoptosis↗
PubMed1999

Vascular endothelial growth factor expression in human neuroblastoma: up-regulation by hypoxia.

Enhanced angiogenesis apparently contributes to the poor clinical outcome of human neuroblastoma, but the mechanisms have remained unclear. We report here that cultured human neuroblastoma cells express a bioactive endothelial cell growth factor indistinguishable from the angiogenesis stimulator vascular endothelial growth factor (VEGF). VEGF is present in neuroblastoma but not vascular endothelial cells, whereas the corresponding VEGF receptors (Flt-1 and Flk-1/KDR) are expressed in endothelial but not neuroblastoma cells. Exposure of neuroblastoma cells to hypoxia induces a marked increase in bioactive VEGF. VEGF is also present in human neuroblastoma specimens, with substantial amounts in apparently hypoxic neuroblastoma cells, eventually accumulating in tumor microvessels. Our results indicate that VEGF (i) is present in human neuroblastomas, (ii) is up-regulated by tumor hypoxia and (iii) may stimulate neuroblastoma angiogenesis by paracrine mechanisms, thereby contributing to the progression of human neuroblastomas. We suggest that inhibition of VEGF activity may represent a novel approach for the therapy of human neuroblastoma.

Cell Division↗
PubMed1999

Down-regulation of endothelial cell growth inhibitors by enhanced MYCN oncogene expression in human neuroblastoma cells.

Recent evidence indicates that the genetic alterations of the multistage process of malignant transformation appear to activate tumor neovascularization by altering the balance between stimulators and inhibitors of angiogenesis. In the present study, we have attempted to define the effect of enhanced MYCN oncogene expression on the profile of endothelial cell growth modulators in neuroblastoma cells. We report here that conditioned medium of human neuroblastoma cells with normal MYCN expression contains three inhibitors of endothelial cell proliferation, which appear to be novel proteins as judged by their physicochemical, immunological and biological properties. All three inhibitors are diminished or become undetectable upon experimental increase of MYCN expression. Our results suggest that enhanced MYCN expression in human neuroblastoma cells alters the angiogenic balance by down-regulating endothelial cell growth inhibitors but leaving the expression of the stimulators unaffected. These data shed light on the molecular mechanisms linking the genetic changes of malignant transformation with initiation of tumor angiogenesis. Moreover, our observations might explain the poor prognosis of human neuroblastomas following MYCN oncogene amplification through initiation of angiogenesis and subsequent tumor growth and spread.

Cell Division↗
PubMed1996

Ionised and total magnesium serum concentrations in renal and hepatic diseases.

Ionised and total magnesium concentrations were determined in the serum of different groups of patients suffering from renal or hepatic diseases. Ionised magnesium was measured by Microlyte 6 (KONE, Espoo, Finland) and total magnesium by atomic absorption spectrometry. In renal insufficiency ionised and total magnesium concentrations were almost equally increased. In proteinuria with a normal glomerular filtration rate, "pseudohypomàgnesaemia" was observed, i.e. decreased total magnesium concentration in parallel with a decreased albumin concentration with no significant change in the concentration of ionised magnesium. Hypermagnesaemia occurred in liver diseases combined with renal insufficiency, whereas "pseudohypomagnesaemia" was most often found in the absence of renal failure. Also treatment with an aldosterone antagonist was associated with a normal ionised magnesium concentration, but the total magnesium concentration was decreased; when additional magnesium was administered, the total magnesium concentration approached a normal value, while ionised magnesium slightly exceeded reference values. Only during cyclosporin treatment did both ionised and total magnesium concentrations become lowered. However, the decrease of total magnesium exceeded that of ionised magnesium due to concomitant hypoalbuminaemia with reduction of the protein-bound fraction. It is concluded that especially low total magnesium concentrations should be investigated by measurement of ionised magnesium to exclude "pseudohypomagnesaemia".

Adolescent↗
PubMed1993

Antiretroviral therapy in sporadic adult amyotrophic lateral sclerosis.

Clinical and experimental findings in idiopathic amyothrophic lateral sclerosis (ALS) would be compatible with a retroviral involvement. In 35 adult patients with non-familial ALS we observed elevated circulating immune complexes, a decrease in IgG3 isotype and enzyme-linked sorbent assay (ELISA) serum antibodies against human spuma retrovirus (HSRV), confirmed by specific human foamy virus immunoblots. All 35 were negative for IgM or relevant IgG anti-ganglioside antibodies. We treated 12 HIV-negative, immune-complex-positive ALS patients with 500 mg d-1 zidovudine p.o. over 2-10 months and found reductions of serum creatine kinase and circulating immune complexes from two days to two weeks after the beginning of medication.

Adult↗
PubMed1992

Human spumavirus antibodies in sera from African patients.

Serum samples collected from patients with a wide variety of diseases from African and other countries were tested for antibodies to the human spumaretrovirus (HSRV). A spumaviral env-specific ELISA was employed as screening test. Out of 3020 human sera screened, 106 were found to be positive (3.2%). While the majority of patients' sera from Europe (1581) were negative, 26 were positive (1.6%). Sera from healthy adult blood donors (609), from patients with multiple sclerosis (48), Graves' disease (45), and chronic fatigue syndrome (41) were negative or showed a very low prevalence for spumaviral env antibodies. A higher percentage of seropositives (6.3%) were found among 1338 African patients from Tanzania, Kenya, and Gabon. Out of 1180 patients from Tanzania, 708 suffered from tumors, 75 from AIDS, and 128 had gynecological problems; 51 of the Tanzanian patients were HSRV seropositive (4.3%). A particularly high percentage of 16.6% seropositives were identified among nasopharyngeal carcinoma patients (NPC) from Kenya and Tanzania consistent with results reported 10 years ago. However, 20 nasopharyngeal carcinoma patients from Malaysia were HSRV-seronegative. In selected cases, sera from seropositive individuals were reacted with proteins from HSRV-infected cells in vitro. HSRV env- and gag-specific antibodies were specifically detected by these sera in Western blots. The results indicate spumavirus infections in human patients with various diseases at a relatively low prevalence worldwide; in African patients, however, the prevalence of spumavirus infections is markedly higher.

Africa↗