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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Morphological alterations in the structure of undifferentiated and morphologically differentiated human neuroblastoma cells induced by phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C, were examined by video microscopy and immunomorphology. In undifferentiated cells, PMA induced the formation of motile actin-rich lamellas and of stable cylindrical processes rich in microtubules. Formation of stable processes resulted either from the collapse of lamellas or the movement of the cell body away from the base of a process. In differentiated cells, PMA induced the rapid extension of small lamellas and subsequent formation of short-lived elongated processes from the lateral edges of neurites. Additionally, growth cones exhibited enhanced modulation in shape after PMA treatment. These reversible reorganizations were similar to the actinoplast-tubuloplast transformations exhibited by PMA-treated fibroblasts. We suggest that actinoplast-tubuloplast reorganizations play essential roles in morphogenesis where stable cytoplasmic extensions are induced by external stimuli. In particular, PMA-induced reorganizations of neural cells in culture may be a model for morphological modulations that occur in nerve tissue.
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PMID:Reversible structural alterations of undifferentiated and differentiated human neuroblastoma cells induced by phorbol ester. 151 42

Phrenic nerve palsy (PNP) is seen in infants and young children usually resulting from operative trauma or birth injury. Spontaneous recovery usually occurs, but occasionally surgical plication is necessary. Twenty-three cases of PNP over a 10-year period were managed surgically. Patient ages ranged from 1 day to 30 months (median, 4 months), 18 were male and five female. Cause was operative trauma in 18 (17 cardiac surgery, one neuroblastoma), birth trauma in two, and idiopathic in three. The right side was involved in 14, the left in eight, and both in one. Indications for plication were inability to wean from the ventilator (group 1, 16 patients), recurrent pneumonia (group 2, four patients), and respiratory distress (group 3, three patients). The 16 patients in group 1 were intubated for a median of 18.5 days from onset of PNP to plication. Postoperatively, three had continuing congestive heart failure (one died at 16 days of age, one was still chronically ventilated at 22 months, one was extubated at nine days); the other 13 were extubated at a median of two days postoperatively. All the patients in groups 2 and 3 were extubated within two days of surgery. Twelve plications were transthoracic and 11 were transabdominal. Postoperative complications included pneumonia (2), wound infection (1), pneumothorax (2), and mucous plug with pulmonary collapse (1). One patient died of cardiac failure at 16 days. One patient in group 3 developed recurrent respiratory distress 4 months postoperatively; he had a recurrent elevated hemidiaphragm requiring a second plication.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plication of the diaphragm for infants and young children with phrenic nerve palsy. 317 45

The contribution to the clinical picture of eosinophilic granuloma of the spine. This tumor-like, osteolytic bone lesion presents both diagnostic and therapeutic problems. Solitary eosinophilic granuloma of the spine is not common. Compared to the multiple manifestation of eosinophilic granuloma, which seldom spares the spine, vertebral involvement is rare in cases of solitary eosinophilic granuloma (about 10 p.c.). Spinal involvement of this disease is mainly characterized by an undramatic, uneventful clinical course, even in cases of extensive osteolytic bone defects, varying laboratory findings as well as partial or complete collapse of a vertebra, mostly in form of a true vertebrae plana. Open biopsy is recommended instead of needle aspiration biopsy in solitary eosinophilic granuloma of the spine in order to exclude Ewing's sarcoma, neuroblastoma, or bony manifestations of leukemia. In cases of solitary eosinophilic granuloma various therapeutic methods have been tried. Some authors have registered good results by means of prolonged immobilization, similar to fracture treatment. Others have used radiation therapy in moderate doses. We suggest operative treatment of solitary eosinophilic granuloma. Our procedure comprises open biopsy, frozen section examination, and curettage of the affected vertebral body, taking care not to destroy the epiphyseal plate or the intervertebral disc. Vertebral body replacement is achieved by means of a bone graft, taken from the iliac crest. The original height of the vertebra is thus restored and immediate stability of the involved area guaranteed. Undisturbed bone growth of the end plated of the vertebral body can be observed. This technique is to prevent disturbances of spinal growth and permanent deformities.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Eosinophilic granuloma of the spine]. 401 83

It has been suggested that G0 and Gi play a role in the collapse of axonal growth cones and the retraction of neurites. We have studied the G-protein content of neuroblastoma cells undergoing neurite outgrowth and subsequent retraction in response to neocarzinostatin (NCS). Stimulators of G0 and Gi have no effect upon neurite outgrowth or retraction and the cellular content of G0 and Gi does not change during the course of these morphological phenomena. Modulation of G-protein content, therefore, most likely does not play a role in this process.
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PMID:G-protein expression during enediyne-induced neurite outgrowth in neuroblastoma. 775 74

The neuronal growth-associated protein GAP-43 is expressed maximally during development and regeneration, and is enriched at the cytosolic surface of the growth cone membrane. GAP-43 can activate the GTP-binding protein G(o) which is also a major component of the growth cone membrane. These findings have led to the hypothesis that GAP-43 might modulate neurite outgrowth by altering G-protein activity. Here we define the sequence requirements for GAP-43 amino terminal peptide stimulation of G(o), and test these peptides as potential modulators of neurite outgrowth. The first 10 amino acids of GAP-43, Met-Leu-Cys-Cys-Met-Arg-Arg-Thr-Lys-Gln, stimulate G(o). Substitutions at particular residues reveal that cys3, cys4, arg6, and lys9 are critical, but arg7 is not. Both the GAP-43(1-10) peptide and the G-protein-activating peptide mastoparan induce growth cone collapse and inhibit neurite extension from embryonic chick dorsal root ganglion and retinal neurons. This is likely to be mediated by G-proteins: pertussis toxin blocks the inhibition, and mutant peptides that do not activate G(o) do not alter outgrowth. In contrast to the case with embryonic chick dorsal root ganglion cells, neurite outgrowth from N1E-115 neuroblastoma cells is stimulated by GAP-43(1-10). This is probably also a G-protein-mediated event because it is blocked by pertussis toxin, because the sequence requirements match those for G(o) stimulation, and because mastoparan stimulates outgrowth from these cells. The longer GAP-43(1-25) peptide does not alter neurite outgrowth unless the cells are permeabilized, suggesting an intracellular site of action. These data identify a novel set of compounds that modulate neurite outgrowth, and also support the notion that GAP-43 can alter neurite extension by modulating pertussis toxin-sensitive G-protein activity in the growth cone.
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PMID:GAP-43 amino terminal peptides modulate growth cone morphology and neurite outgrowth. 808 50

The concentration of free calcium ions in the cytosol has been shown to influence many components of growth cone behaviour, including the extension of filopodia and veils, the addition of new membrane to the plasmalemma, the retraction and disappearance of filopodia, and gross collapse and retraction of the growth cone. A spatially localized modulation of these processes by very local calcium changes has been proposed to underlie the steering of growth cones by gradients of neurotransmitters, voltage and cell adhesion molecules. Such local control can be studied in mouse neuroblastoma cells, where depolarization causes calcium to rise in a limited number of spatially restricted hotspots, triggering a localized advance. We have studied the simple, club-shaped growth cones that are characteristically found on advancing neurites. Depolarization caused calcium to increase most at the distal, leading tip. Agents that disrupt calcium-induced calcium release do not affect growth cone calcium dynamics, ruling out a local release of calcium at the tip as a cause of the gradient. Using cell-attached patch recording, we find that L-type calcium channels are present at a higher density at the distal tip than in the proximal growth cone. Our results show that the calcium gradients seen in depolarized growth cones are a direct consequence of a gradient of calcium channel density.
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PMID:Calcium channels in neuroblastoma cell growth cones. 896 37

Rho family GTPases have been assigned important roles in the formation of actin-based morphologies in nonneuronal cells. Here we show that microinjection of Cdc42Hs and Rac1 promoted formation of filopodia and lamellipodia in N1E-115 neuroblastoma growth cones and along neurites. These actin-containing structures were also induced by injection of Clostridium botulinum C3 exoenzyme, which abolishes RhoA-mediated functions such as neurite retraction. The C3 response was inhibited by coinjection with the dominant negative mutant Cdc42Hs(T17N), while the Cdc42Hs response could be competed by coinjection with RhoA. We also demonstrate that the neurotransmitter acetylcholine (ACh) can induce filopodia and lamellipodia on neuroblastoma growth cones via muscarinic ACh receptor activation, but only when applied in a concentration gradient. ACh-induced formation of filopodia and lamellipodia was inhibited by preinjection with the dominant negative mutants Cdc42Hs(T17N) and Rac1(T17N), respectively. Lysophosphatidic acid (LPA)-induced neurite retraction, which is mediated by RhoA, was inhibited by ACh, while C3 exoenzyme-mediated neurite outgrowth was inhibited by injection with Cdc42Hs(T17N) or Rac1(T17N). Together these results suggest that there is competition between the ACh- and LPA-induced morphological pathways mediated by Cdc42Hs and/or Rac1 and by RhoA, leading to either neurite development or collapse.
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PMID:Rho family GTPases and neuronal growth cone remodelling: relationship between increased complexity induced by Cdc42Hs, Rac1, and acetylcholine and collapse induced by RhoA and lysophosphatidic acid. 903 47

The action of arthropod venoms is important to predators in search of prey and to humans as incidental victims or as a source for pharmacologically active compounds. Venoms from 30 arthropods (including 26 spider species) were assessed for cytotoxicity using cultured cells from one insect (Sf9) and three mammalian (murine neuroblastoma and macrophages and human osteosarcoma) sources. The most cytotoxic venoms to the four cell lines were from predatory jumping spiders (Salticidae, Phidippus sp.) and a centipede (Scolopenra sp.), with concentrations for 50% response of 1-8 microg venom per ml. The cytotoxicity of Phidippus ardens venom at these levels was instantaneous and evidenced by dramatic disruption of cell membranes resulting in cell collapse.
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PMID:Cytotoxic effects of arthropod venoms on various cultured cells. 962 May 82

The degradation of alphaII- and betaII-spectrin during apoptosis in cultured human neuroblastoma SH-SY5Y cells was investigated. Immunofluorescent staining showed that the collapse of the cortical spectrin cytoskeleton is an early event following staurosporine challenge. This collapse correlated with the generation of a series of prominent spectrin breakdown products (BDPs) derived from both alphaII- and betaII-subunits. Major C-terminal alphaII-spectrin BDPs were detected at approximately 150, 145, and 120 kDa (alphaII-BDP150, alphaII-BDP145, and alphaII-BDP120, respectively); major C-terminal betaII-spectrin BDPs were at approximately 110 and 85 kDa (betaII-BDP110 and betaII-BDP85, respectively). N-terminal sequencing of the major fragments produced in vitro by caspase 3 revealed that alphaII-BDP150 and alphaII-BDP120 were generated by cleavages at DETD1185*S1186 and DSLD1478*S1479, respectively. For betaII-spectrin, a major caspase site was detected at DEVD1457*S1458, and both betaII-BDP110 and betaII-BDP85 shared a common N-terminal sequence starting with Ser1458. An additional cleavage site near the C terminus, at ETVD2146*S2147, was found to account for betaII-BDP85. Studies using specific caspase or calpain inhibitors indicate that the pattern of spectrin breakdown during apoptosis differs from that during non-apoptotic cell death. We postulate that in concert with calpain, caspase rapidly targets critical sites in both alphaII- and betaII-spectrin and thereby initiates a rapid dissolution of the spectrin-actin cortical cytoskeleton with apoptosis.
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PMID:Simultaneous degradation of alphaII- and betaII-spectrin by caspase 3 (CPP32) in apoptotic cells. 971 74

Apoptosis and aging share common mechanisms in oxidative stress and mitochondrial involvement. Treatment of cultured neuroblastoma cells with a radical initiator induced apoptosis; raise in hydrogen peroxide and release of cytochrome c from mitochondria preceded collapse of mitochondrial potential and cell death. In rat hepatocytes treated with adriamycin incubation with exogenous Coenzyme Q10 counteracted the drug-induced increase of hydrogen peroxide and the fall of the mitochondrial potential, thus demonstrating the quinone antioxidant effect. Complex I activity and its rotenone sensitivity decreased in brain cortex non-synaptic mitochondria from old rats; a 5 kb mitochondrial DNA deletion was found only in the old rats. A similar behavior was found in human platelets from old individuals. The postulated energy decline was confirmed by the inhibitor sensitivities of platelet aggregation and lactate production. The lack of the 5 kb deletion in platelets throws doubts on mitochondrial DNA lesions as the only causes of mitochondrial dysfunction in aging.
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PMID:Oxidative stress, antioxidant defences and aging. 991 19


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