Preferencje help
Polish version English version Język
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 23

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 2 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

Wyszukiwano:
w słowach kluczowych:  neuroblastoma
help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 2 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
1
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Correlation between N-myc amplification and other prognostic markers in children with neuroblastoma

100%
Januszkiewicz-Lewandowska D.
Genetica Polonica
|
1993
|
tom 34
|
nr 4
373-378
2

Characterisation of hypoxanthine-guanine phosphoribosyltransferase-deficient [HGPRT-] neuroblastoma: models for Lesch-Nyhan syndrome

100%
Ma M. H. Y., Stacey N. C., Korenevsky A. V., Duley J. A., Connolly G. P.
Cellular and Molecular Biology Letters
|
1999
|
tom 04
|
nr 3
3

(Anty)angiogeneza w nerwiaku zarodkowym współczulnym u pacjentów pediatrycznych

88%
Sujka-Kordowska P., Malinska A., Zabel M.
Postępy Biologii Komórki
|
2017
|
tom 44
|
nr 1
4

Catecholamine content of neuroblastoma: modelling Lesch-Nyhan syndrome [LNS]

88%
Korenevsky A. V., Duley J. A., Connolly G. P.
Cellular and Molecular Biology Letters
|
1999
|
tom 04
|
nr 3
5

Perspektywy zastosowania immunoterapii w leczeniu neuroblastoma

75%
Horwacik I.
Postępy Biologii Komórki
|
2005
|
tom 32
|
nr 1
97-109
6

Nerwiak zarodkowy [neuroblastoma] - znaczenie wynikow badan cytogenetycznych i molekularnych w ustaleniu strategii leczenia i rokowania

75%
Lipska B. S., Limon J.
Postępy Biologii Komórki
|
2005
|
tom 32
|
nr 1
59-76
7

N-acetylaspartate in zinc exposed cholinergic SN56 neuroblastoma cells

75%
Zysk M., Ronowska A., Bielarczyk H., Szutowicz A.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Cholinergic neurons of brain septum were found to be highly susceptible to neurodegenerative conditions. The sources of this particular sensitivity remain unclear. There is suggestion that their low resistance to cytotoxic conditions might be due to comprehensive consumption of acetyl-CoA. In cholinergic neurons the acetyl-CoA, except of intramitochondrial utilization for energy and NAA synthesis, serves as a precursor of acetycholine in their cytoplasmic compartment. The later pathway, present only in cholinergic neuronal cells, can cause temporary shortages of acetyl-CoA under cytotoxic conditions. The aim of our study was to investigate how these conditions affect N-acetylaspartate (NAA) synthesis as another acetylCoA consuming pathway in cholinergic SN56 neuroblastoma cells. These cells are recognized in vitro model of brain cholinergic neurons. Neurodegenerative conditions were induced by chronic exposition SN56 cells to zinc, a known excitotoxic agent. NAA in cholinergic neuroblastoma cells was assayed by HPLC preceded by one-dimension solid phase/ion exchange extraction. Levels of NAA in nondifferentiated (NC) and differentiated (DC) cells were equal to 70 and 56 nmol/mg protein, whereas rates of its release were 21.6 and 20.5 nmol/h/mg protein. Levels of acetyl-CoA and activities of choline acetyltransferase in NC and DC were equal to 29.5 and 23.8 pmol/mg of protein and to 0.106 and 0.232 nmol/min/ mg of protein, respectively. It indicates that 20% decrease of acetylCoA level in DC was caused by its increased utilization for acetylcholine synthesis. Zinc inhibited TCA cycle enzymes and pyruvate dehydrogenase activities at [IC50] values well below 0.10 mmol/L. Despite of that zinc concentrations up to 125 µM increased levels of acetyl-CoA and NAA both in DC and NC by 94 and 57% and by 27% and 22%, respectively. However, 0.175 mmol/L Zn resulted in impairment of 27 and 36% of NC and DC, as measured by lactate dehydrogenase release, respectively. In these conditions levels of acetyl-CoA in NC and DC were decreased by 68% and 45%, respectively. NAA levels were also suppressed by 63% and 51%, respectively. These data indicate the existence of significant, although differential interrelationships between rates of acetyl-CoA synthesis in mitochondria of cholinergic neurons and its utilization for NAA and acetylcholine synthesis. Increased acetylcholine synthesis may contribute to greater susceptibility of cholinergic neurons to cytotoxic conditions. On the other hand, NAA synthesis may not be a factor decreasing availability of acetyl-CoA in neurons with high expression of cholinergic phenotype. Its alterations seem to be secondary to respective shifts in acetyl-CoA levels. Supported by project IP2010035370 Ministry of Science and Higher Education.
8

Cytokine action and oxidative stress response in differentiated neuroblastoma SH-SY5Y cells

75%
Kania J., Baranska A., Guzdek A.
Acta Biochimica Polonica
|
2003
|
tom 50
|
nr 3
In the retinoic acid-differentiated neuroblastoma SH-SY5Y cells, IL-1 induced bind­ing activity of NFkB and up-regulated the expression and activity of MnSOD. The IL-1-elicited effects were partly reversed by IL-4 and IL-6. It is proposed that IL-4 and IL-6 may participate in the regulation of the imbalanced oxidant status induced by IL-1 in differentiated neuroblastoma cells. In the SH-SY5Y cell line, TNFa neither ac­tivated NFkB nor induced MnSOD expression and activity, but was capable of modu­lating the IL-1 effects. Pyrrolidine dithiocarbamate (PDTC), an inhibitor of NFkB acti­vation, down-regulated the expression and activity of MnSOD, which may suggest that the regulation of MnSOD by IL-1 in retinoic acid-differentiated neuroblastoma cells was mediated by the nuclear factor kB.
9

Vascular endothelial growth factor [VEGF]-C - a potent risk factor in children diagnosed with stadium 4 neuroblastoma

63%
Nowicki M., Konwerska A., Ostalska-Nowicka D., Derwich K., Miskowiak B., Kondraciuk B., Samulak D., Witt M.
Folia Histochemica et Cytobiologica
|
2008
|
tom 46
|
nr 4
493-499
10

Izolacja wirusa wscieklizny na komorkach mysiej neuroblastomy

63%
Molenda J., Otachel-Hawranek J.
Medycyna Weterynaryjna
|
1998
|
tom 54
|
nr 12
823-825
Two official methods are most commonly employed in laboratory proceedings aimed at confirming the existence of rabies in animals: the fluorescent antibody test (FAT) and mouse innoculation test. Introducing the rabies tissue culture infection test (RTCIT), that serves to multiply the virus into cell culture may improve and reduce laboratory procedure time. In our examination we managed to detect the virus in naturally and experimentally infected animals. The method proved to be as efficient as the mouse inoculation test, but its results could be obtained more rapidly. The advantages and limitations of the test are discussed in this article.
11

The knockdown of c-myc expression by RNAi inhibits cell proliferation in human colon cancer HT-29 cells in vitro and in vivo

63%
Zhang X., Ge Y.-L., Tian R.-H.
Cellular and Molecular Biology Letters
|
2009
|
tom 14
|
nr 2
305-318
We investigated the effects of RNA interference-mediated silencing of the c-myc gene on celluar proliferation and apoptosis in human colon cancer HT-29 cells in vitro and in vivo. A small interfering RNA (siRNA) targeting c-myc was designed, the DNA template was synthesized, and the siRNA was obtained by in vitro transcription. After siRNA transfection into HT-29 and human neuroblastoma IMR-32 cells with Lipofectamine 2000™, the proliferation of the HT-29 and IMR-32 cells was assessed via 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) colorimetry, and Hoechst 33258 staining was used to observe cell apoptosis. Following gene transfer to HT-29 cells, the expression of c-myc mRNA was examined via reverse transcription polymerase chain reaction, and the level of the protein via Western blot assay. Growth curves were constructed and in vivo experiments were performed on nude mice to assess the effects of c-myc silencing on tumor growth. The c-myc expression in the tumor tissue was measured by reverse transcription polymerase chain reaction and subsequently by immunohistochemistry. Our paper demonstrates that the delivery of siRNA directed against c-myc not only efficiently down-regulated the expression of c-myc, inhibited the proliferation of HT-29 cells and induced apoptosis in vitro, but also suppressed the growth of colon cancer cells in vivo.
12

New method for quantitative analysis of GD2 ganglioside in plasma of neuroblastoma patients

63%
Czaplicki D., Horwacik I., Kowalczyk A., Wieczorek A., Bolek-Marzec K., Balwierz W., Kozik A., Rokita H.
Acta Biochimica Polonica
|
2009
|
tom 56
|
nr 3
423-431
 Neuroblastoma, the most common extracranial solid tumour of childhood, is a malignancy of unknown origin and non-specific symptoms. One of the markers of the disease is GD2 ganglioside (disialoganglioside), which is abundantly expressed on the surface of neuroblastoma cells. Gangliosides are known to be shed by tumour cells and this phenomenon can be significant in cancer progression as they inhibit a number of immune responses both in vitro and in vivo. In search for novel markers useful in monitoring and prognosis of neuroblastoma, we developed and validated a new quantitative method of GD2 ganglioside analysis in human blood plasma. We evaluated the level of gangliosides in blood serum of 34 neuroblastoma patients using high-performance liquid chromatography. The technique was used to detect fluorescently labelled oligosaccharides derived from serum glycosphingolipids by enzymatic digestion with ceramide glycanase. The developed method allowed determination of GD2 concentrations at the picomole level and required only 40 μl of plasma, which should be particularly useful when the quantity of clinical material is limiting. Moreover, this method can be applied to study concentration of other gangliosides, as shown for GD3 ganglioside. Analysis of plasma samples from the 34 neuroblastoma patients did not reveal any correlations between the concentration of GD2 ganglioside and clinical parameters, including the results of therapy; it showed, however, that the concentration of GD2 ganglioside in the plasma of neuroblastoma patients decreased substantially in the course of treatment.
13

Comparison of the cell immunophenotype of metastatic and primary foci in stage IV-S neuroblastoma

63%
Nowicki M., Miskowiak B.
Folia Histochemica et Cytobiologica
|
2002
|
tom 40
|
nr 3
14

Abnormal intracellular signalling in skin fibroblasts from LNS patients and HGPRT-deficient neuroblastoma

63%
Hussain S. P., Alexander N., Duley J. A., Connolly G. P.
Cellular and Molecular Biology Letters
|
1999
|
tom 04
|
nr 3
15

Morphogenesis of B103 neuroblastoma and B103-4C its mutant derivative: modelling Lesch-Nyhan syndrome

63%
Ma M. H. Y., Stacey N. C., Duley J. A., Connolly G. P.
Cellular and Molecular Biology Letters
|
1999
|
tom 04
|
nr 3
16

Translocation of polysialic acid across liposomal membranes: energy barrier model and electron microscopy studies

63%
Janas T., Krajinski H., Janas T.
Cellular and Molecular Biology Letters
|
1999
|
tom 04
|
nr 2
17

Serum acute phase proteins in neuroblastoma children at diagnosis and during the clinical treatment. A preliminary report

51%
Lipinska L., Laskowska-KLita T., Izbicki T.
Folia Histochemica et Cytobiologica
|
1992
|
tom 30
|
nr 4
18

Carnitine - a known compound, a novel function in neural cells

51%
Nalecz K. A., Nalecz M. J.
Acta Neurobiologiae Experimentalis
|
1996
|
tom 56
|
nr 2
19

Effect of opioids on Ca2plus-cAMP responsive element binding protein

51%
Bilecki W., Przewlocki R.
Acta Neurobiologiae Experimentalis
|
2000
|
tom 60
|
nr 4
Ca2+ /CAMP response element binding protein (CREB) is an important factor linking the opioid-regulated secondary messenger systems to alterations in gene expression. Opioids regulate CREB level, its phosphorylation and binding to its corresponding response element in the promoters of several genes implicated in drug addiction. CREB mediates the action of opioids on the expression of several genes in brain regions responsible for drug-seeking behavior and manifestation of signs of dependence. Moreover, alterations in CREB level can affect the rewarding properties of morphine and regulate the self-administration of cocaine. At the cellular level CREB acts as convergence point for different cellular pathways. Opioids affect two different intracellular mediator systems: inhibitory - connected with cAMP, and stimulatory - involving calcium and the PKC pathway. Both can affect CREB but in different phases of opiate action. The presence of this biphasic mechanism can explain the phenomenon of the induction of some CRE-controlled genes after both acute and chronic morphine administration. Cellular studies also highlight the relevance of other ATF/CREB family members which can affect Ca /cAMP response element (CRE) controlled transcription as well as other transcription factors which make the opioid induction longer lasting.
20

Lead-induced cell death of human neuroblastoma cells involves GSH deprivation

51%
Chetty C. S., Vemuri M. C., Campbell K., Suresh C.
Cellular and Molecular Biology Letters
|
2005
|
tom 10
|
nr 3
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 2 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.