Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous results obtained in experimental and clinical trials have demonstrated that topical combined thrapy with human interferon (HI) and human colostral secretory immunoglobulin A (S-IgA) is effective against herpetic corneal infection. This therapy prevented encephalitis in rabbits but could not completely prevent recurrences either in rabbits or in patients. A number of in vitro studies were designed to elucidate the role of these factors in herpes simplex virus replication in the nervous system, with the following results: (1) HSV latency in trigeminal ganglia (TG) explanted from rabbits with experimental herpetic keratitis, topically treated with HI or HI/S-IgA: HSV was recovered in 30% TG after 15-19 days co-cultivation on RK-13 cells. (2) HSV replication in nervous ganglia and nerve of newborn rabbits in organ culture; influence of HI or HI plus IgG: a restrictive HSV productive infection was demonstrated in this system, although yields were always higher in nerve cultures. We were unable to demonstrate a direct effect of HI on HSV-1 replication. When explants were treated with HI and IgG before and after infection for 48 hours a delay in the expression of HSV-1 was detected by co-cultivation. (3) Replication of HSV-1 and HSV-2 in a C1300 murine neuroblastoma clone (NB41A3): both HSV types replicated with titres of 10(3.4) for HSV-1 AND 10(4.8) for HSV-2 at 48 hours p.i.; CPE was more marked for HSV-2 at 24 hours. HSV-specific antigens were demonstrated by the immunoperoxidase technique.
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PMID:Interferon in the replication of herpes simplex virus in normal and pathological nerve cells. 22 73

Three cases of opsoclonus in normal neonates are reported. There was no evidence of neuroblastoma, encephalitis, or infantile polymyoclonia. It appears that opsoclonus may occur as a transient phenomenon in healthy infants.
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PMID:Neonatal opsoclonus. 92 40

A further case of opsoclonus with myoclonus is described. When this syndrome occurs in childhood an associated neuroblastoma should be excluded. In the majority of cases at all ages no underlying disease will be found, although a preceding history of minor upper respiratory or gastrointestinal infection may be elicited, suggesting that a possible encephalitis affecting brain stem mechanisms may be the cause. The prognosis is, as a rule, excellent although full recovery may not occur for many months. Corticosteroids and nitrazepam may have a place in the treatment of severely affected patients with distressing symptoms.
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PMID:Opsoclonus with myoclonus. 121 86

In the last decade, several features have improved our knowledge of CNS paraneoplastic syndromes. Patients with paraneoplastic cerebellar degeneration (PCD) and breast or ovarian cancer, but not with other tumors, harbor an antibody against Purkinje cells (called anti-Yo). Clinical features of anti-Yo positive and negative PCD are similar but the latter may have a less progressive clinical course with occasional remissions. In addition to the association of opsoclonus with neuroblastoma, this syndrome has been identified in patients with breast or small-cell lung cancer (SCLC). Patients with opsoclonus and breast cancer have an antineuronal antibody (called anti-Ri) not present if opsoclonus is associated with SCLC or neuroblastoma. Paraneoplastic encephalomyelitis (PEM) is almost always associated with SCLC. Most patients present with sensory neuronopathy, limbic or brainstem encephalitis but involvement of multiple levels is usual. An antibody (called anti-Hu) against neuronal nuclear antigens is present in patients with PEM and SCLC. Autopsy studies demonstrate deposits of anti-Hu specific IgG in the neurons and a predominance of T cells in the inflammatory infiltrates. Treatment of the tumor and immunosuppressors are effective in opsoclonus whereas patients with PCD or PEM with circulating antibodies do not improve.
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PMID:Clinical and pathological advances on central nervous system paraneoplastic syndromes. 144 70

Alphaviruses replicate in a wide variety of cells in vitro. The prototype alphavirus, Sindbis virus, causes an age-dependent encephalitis in mice and serves as an important model system for the study of alphavirus neurovirulence. To begin to understand the role of cellular virus receptors in the pathogenesis of Sindbis virus infection, we developed an anti-idiotypic antibody made in rabbits against a neutralizing monoclonal antibody specific for the E2 surface glycoprotein. The anti-idiotypic antibody (anti-Id 209) bound to N18 mouse neuroblastoma cells and inhibited adsorption of 35S-labeled virus by 50%. Binding of anti-Id 209 was inhibited by pretreatment of N18 cells with various proteases but not with neuraminidase or phospholipase, while virus binding was inhibited by pretreatment with phospholipase as well as protease. Anti-Id 209 precipitated proteins of 110 and 74 kDa from N18 cells intrinsically labeled with [35S]methionine. N18 cells grow with two phenotypes in culture, and immunoprecipitation of 125I-surface-labeled cells showed that the 74-kDa protein was present on loosely adherent cells growing in aggregates, while the 110-kDa protein was present in smaller amounts on firmly adherent cells growing as a monolayer. Analysis of brain cells from newborn mice by flow cytometry showed that all cells expressed the receptor protein at birth, but by 4 days after birth half of the cells had ceased receptor expression. A survey of other cell lines showed the protein to be present on murine fibroblastic and other rodent neuroblastoma cell lines but rarely on human neural or nonneural cell lines. These studies suggest that one of the receptors for Sindbis virus on mouse neural cells is a protein that is regulated during development of the nervous system. Developmental down-regulation of receptor protein expression may contribute to the age-dependent nature of susceptibility of mice to fatal alphavirus encephalitis.
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PMID:Identification of a putative alphavirus receptor on mouse neural cells. 165 82

The combined effects of Acyclovir [9-(2'-hydroxyethoxymethyl)guanine; ACV] and human interferon-alpha (IFN-alpha) on replication of the herpes simplex virus type I (HSV-1) were determined in human neural cell lines, neuroblastoma (IMR), glioblastoma (118MGC), and glioma (U251MG). HSV-1 grew well in all these cells, with final yields of more than 1 x 10(6) PFU/ml. In terms of virus-yield reduction, ACV was found to be highly effective in IMR, moderately effective in U251MG, but ineffective in 118MGC. By contrast, IFN-alpha reduced the virus yield significantly in 118MGC and in U251MG, but did not in IMR. Combined application of ACV and IFN-alpha strongly inhibited the virus replication in all three cell lines with various degrees of synergism or additive effect. These results were also confirmed by immunofluorescent examinations. The sensitivity of HSV-1 to ACV or IFN-alpha was found to be different among the three different cell types. By combining the two agents, the virus growth was strongly suppressed in all the cells. These results suggest the importance of combination therapy for severe type of herpes simplex encephalitis in clinical practice.
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PMID:Combined effects of acyclovir and human interferon-alpha on herpes simplex virus replication in cultured neural cells. 255 47

The matrix (M) genes of Yamagata-1 strain subacute sclerosing panencephalitis virus passaged in African green monkey kidney cells and human neuroblastoma cells displayed strikingly nonrandom sequence divergence. The genes of both substrains shared a large number of uridine (U) to cytidine (C) transitions, but the latter contained numerous additional U to C changes in a localized region. Over 90% of the additional mutations were identical to the hypermutated nucleotides in the M gene found in a measles inclusion body encephalitis case. The nonrandom nature, the apparent host dependency, and the abrupt boundaries of these mutations suggest that these mutations might be caused by an extrinsic biased mutational activity rather than intrinsic polymerase errors. This mutational activity might account for the extraordinarily high C to U ratios in the non-protein-coding regions of both the M and fusion genes of wild-type measles virus.
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PMID:Generalized and localized biased hypermutation affecting the matrix gene of a measles virus strain that causes subacute sclerosing panencephalitis. 258 12

A defective subacute sclerosing panencephalitis (SSPE) virus which had been passaged in human embryonic lung cells was transferred to cultures of three neural cell types: neuroblastoma, oligodendroglioma and glioblastoma. The growth characteristics of the virus in these cells were essentially similar to those in non-neural cells. On the other hand, a marked difference in neurovirulence was noticed for the virus grown in neural cells when examined by intracerebral inoculation into mice. The virus passaged in neuroblastoma and oligodendroglioma cells showed high neurovirulence, inducing an acute encephalitis, whereas the virus passaged in human embryonic lung cells and that in glioblastoma cells did not show neurovirulence. These results suggest that the virus recovered its neurovirulence after passage in certain human neural cells.
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PMID:Growth of defective subacute sclerosing panencephalitis viruses in human neural cells and their neurovirulence in mice. 298 73

The authors report two cases of children suffering from Epilepsia Partialis Continua (EPC). The first case concerned a boy primarily affected by abdominal neuroblastoma and secondarily by bilateral EPC; "pallidal posture" was the prominent clinical feature. An acute measles encephalitis was diagnosed and the CT scan showed necrosis of the putamina. The second case concerned a girl suffering from increased intracranial pressure due to suprasellar craniopharyngioma. Seven days after intervention, Diabetes Insipidus and EPC appeared. Enlargement of rolandic and sylvian spaces and lacunar necrosis of the putamen on the left side were also evident on the CT scan. The authors emphasize the significance of occasional metabolic disturbances, especially natremia, in the development of EPC.
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PMID:Kojewnikow's Epilepsia Partialis Continua: two cases associated with striatal necrosis. 314 49

Neurovirulence of the Onderstepoort strain of canine distemper virus (CDV) adapted to human neural cell lines was determined by the intracerebral inoculation of DDD mice at 3 and 5 weeks of age. Intensity of neurovirulence was estimated by histopathological changes in the central nervous system and clinical symptoms. The original virus propagated in Vero cells induced leptomeningoencephalitis, whereas neuroblastoma-adapted virus induced nerve cell degeneration and mild encephalitis with relatively low morbidity and fatality. In contrast, the viruses adapted to glioblastoma and oligodendroglioma caused high morbidity and fatality. The latter two viruses induced necrotizing encephalopathy including edema and hyperemia. In addition, the glioblastoma-adapted virus induced formation of giant cells. The oligodendroglioma-adapted virus caused demyelination and spongy state associated with degeneration of glial cells and axons. These observations are discussed in regard to a possible correlation between the neurovirulence of CDV in mice and its tropism for neural cells in vitro.
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PMID:Neurovirulence in mice of neural cell-adapted canine distemper virus. 372 59


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