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Induced pluripotent stem cells in modeling and cell-based therapy of amyotrophic lateral sclerosis

100%
Csobonyeiova M., Polak S., Nicodemou A., Danisovic L.
Journal of Physiology and Pharmacology
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2017
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tom 68
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nr 5
2

Evoked cardiac response components in cognitive processing: differential effects of amyotrophic lateral sclerosis

100%
Kaiser J., Wronka E., Barry R. J., Szczudlik A.
Acta Neurobiologiae Experimentalis
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1999
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tom 59
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nr 4
3

Immunoexpression of the selected compounds of the SMN complex in spinal cord neurons in patients with sporadic amyotrophic lateral sclerosis (sALS)

84%
Dziewulska D., Sulejczak D., Chrzanowska H., Ogonowska W., Rafalowska J.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr 1
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease leading to degeneration and loss of motoneurons in the spinal cord anterior horns. Although etiology of the disease is unknown there is a hypothesis assuming that survival motor neuron protein (SMN) may save motoneurons from degeneration not only in spinal muscular atrophy (SMA) but also in ALS. In animal models of ALS the neuroprotective role of SMN was observed but it is not known whether the phenomenon is present in humans. Therefore we decided to examine immunoexpression of SMN and functionally associated with it gemin 2, 3 and 4 in the anterior horn neurons of patients with sporadic form of ALS (sALS). Material and methods: The material was composed of 10 spinal cords of patients with sALS who died at the age of 52–87 years 1–8 years after the onset of the disease. On formalin-fixed and paraffin-embedded spinal cords immunohistochemistry was applied. The immunohistochemical reactions were performed with antibodies against SMN and gemin 2, 3 and 4 according to the avidin-biotin-peroxidase method. Results: In all the examined cases expression of SMN and gemin 3 in spinal cord neurons was found although intensity of the immune reactions was diverse. The immunolabel were the most intense in patients with acute course of sALS and gradually decreased with longevity of the disease. Not only motoneurons but also interneurons and sensory neurons revealed immunoexpression of SMN and gemin 3. The immune reaction to gemin 2 was negative. The immunoreactivity for gemin 4 was also negative or very weak. Conclusions: (1) In humans, expression of SMN and gemin 3 in neurons is present through the whole lifespan. (2) In sALS, expression of gemin 2 and 4 is abnormal: absent or diminished respectively. (3) Presence of all components of the SMN-gemin complex is probably necessary for its normal functioning. (4) Since the immunoreactivity for SMN, and gemin 2, 3 and 4 was similar in all the examined cases and 6 from the 10 cases were at the age of 65–87 years it seems that advanced age has no influence on expression of the investigated proteins. This study was supported by the Ministry of Science and Higher Education grant NN 401 014640
4

Immunoreactivities of some proteins forming SMN protein complex within spinal cord in rat model of fALS

84%
Rafalowska J., Sulejczak D., Gadamski R., Wojda R., Mordzewska-Lewczuk M., Dziewulska D.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr 1
Introduction: Amyotrophic lateral sclerosis (ALS) is a major neurodegenerative disease to afflict the adult human population. ALS causes a progressive motoneuron degeneration within anterior horns of the spinal cord. Recent data indicate the presence of mutations in the SMN (Survival Motor Neuron) gene that cause a deficits in the level of the functional SMN protein and may be an exacerbating factor in the disease development of rat model of fALS. SMN forms the multiprotein complex with selected gemins (i.a. gemin 2, 3 and 4). It is known, that the complex is important for motoneuron development in ontogenesis as well as in the proper functioning of mature motoneuron. However, the level of the SMN and individual gemin expression during the life both in humans and rats still become uncovered. The aim of our study was to determine the immunoreactivities of SMN and gemins 2, 3 and 4 in rat model of fALS during all life span. Material and method: Male rats mutated in SOD-1 were subjected to experiments. Animals at age of 60 days (group 1), 90 days (group 2), 120 days (group 3) were asymptomatic. The last group involving symptomatic rats was created from animals older than 120 days. Rats were perfused in deep anaesthesia. The spinal cords were removed and processed in routine histological staining techniques as well as in immunohistochemical methods (to detect SMN and selected gemins proteins). Labelling sections of spinal cords were analyzed with light and fluorescent microscope. Result: SMN and all investigated gemins were present in spinal cord motoneurons in rats from all experimental groups. However, the level of staining was weaker in the paretic rats. In the opposition to other examined proteins the immunoreaction of gemin 2 was weaker starting from 90 day of life. Conclusion: The SMN protein complex is present in motoneurons within the spinal cord during all animal lifespan in the rat model of familiar ALS. This study was supported by the Ministry of Science and Higher Education grant NN 401 014640
5

Effects of biofeedback training on esophageal peristaltis in amyotrophic lateral sclerosis [ALS] patients with dysphagia

84%
Lorens K., Tomik B., Pichor A., Szczudlik A., Sliwowski Z., Konturek S. J.
Journal of Physiology and Pharmacology. Supplement
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2001
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tom 52
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nr 2
6

Stroke, myocardial infarction, acute and chronic inflammatory diseases: caspase and other apoptotic molecules as targets for drug development

84%
Kreuter M., Langer C., Kerkhoff C., Reddanna P., Kania A. L., Maddika S., Chlichlia K., Bui T. N., Los M.
Archivum Immunologiae et Therapiae Experimentalis
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2004
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tom 52
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nr 3
7
Content available remote

Melatonin defeats neurally-derived free radicals and reduces the associated neuromorphological and neurobehavioral damage

67%
Reiter R. J., Tan D.-X., Manchester L. C., Tamura H.
Journal of Physiology and Pharmacology. Supplement
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2007
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tom 58
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nr 6
8
Content available remote

Evaluation of matrix metalloproteinases in serum of patients with amyotrophic lateral sclerosis with pattern recognition methods

67%
Sokolowska B., Jozwik A., Niebroj-Dobosz I., Janik P., Kwiecinski H.
Journal of Physiology and Pharmacology. Supplement
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2009
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tom 60
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nr 5
9

Activation of the heat shock response in a primary cellular model of motoneuron neurodegeneration - evidence for neuroprotective and neurotoxic effects

67%
Kalmar B., Greensmith L.
Cellular and Molecular Biology Letters
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2009
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tom 14
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nr 2
Pharmacological up-regulation of heat shock proteins (hsps) rescues motoneurons from cell death in a mouse model of amyotrophic lateral sclerosis. However, the relationship between increased hsp expression and neuronal survival is not straightforward. Here we examined the effects of two pharmacological agents that induce the heat shock response via activation of HSF-1, on stressed primary motoneurons in culture. Although both arimoclomol and celastrol induced the expression of Hsp70, their effects on primary motoneurons in culture were significantly different. Whereas arimoclomol had survival-promoting effects, rescuing motoneurons from staurosporin and H2O2 induced apoptosis, celastrol not only failed to protect stressed motoneurons from apoptosis under same experimental conditions, but was neurotoxic and induced neuronal death. Immunostaining of celastrol-treated cultures for hsp70 and activated caspase-3 revealed that celastrol treatment activates both the heat shock response and the apoptotic cell death cascade. These results indicate that not all agents that activate the heat shock response will necessarily be neuroprotective.
10

BDNF and NT-3 widen the scope of neurotrophin activity: Pharmacological implications

67%
Skup M. H.
Acta Neurobiologiae Experimentalis
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1994
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tom 54
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nr 2
11

Thalidomide-based TNF-alpha inhibitors for neurodegenerative diseases

67%
Greig N. H., Giordano T., Zhu X., Yu Q., Perry T. A., Holloway H. W., Brossi A., Rogers J. T., Sambamurti K., Lahiri D. K.
Acta Neurobiologiae Experimentalis
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2004
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tom 64
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nr 1
12
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Content available

Ryby i owoce morza jako źródło narażenia człowieka na metylortęć

43%
Mania M., Wojciechowska-Mazurek M., Starska K., Rebeniak M., Postupolski J.
Roczniki Państwowego Zakładu Higieny
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2012
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tom 63
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nr 3
Ryby i owoce morza są zalecanymi składnikami diety, dostarczają one pełnowartościowego białka, witamin, soli mineralnych oraz kwasów tłuszczowych omega-3. Te środki spożywcze mogą być również źródłem pobrania metylortęci przez ludzi. Artykuł ten zawiera informacje na temat źródeł narażenia na organiczne połączenia rtęci, toksyczności, metabolizmu oraz przemian rtęci w środowisku. Przedstawiono zalecenia żywieniowe przygotowane przez Komisję Europejską i państwa członkowskie w odniesieniu do spożycia ryb drapieżnych, uwzględniające najbardziej wrażliwe grupy populacji, takie jak: kobiety planujące ciążę, ciężarne, karmiące matki oraz dzieci. Na podstawie piśmiennictwa omówiono również zanieczyszczenie ryb i owoców morza rtęcią i metylortecią. Opisano rolę selenu jako czynnika, który obniża toksyczność metylortęci jak również przedstawiono informacje o potencjalnych czynnikach etiologicznych związanych z chorobą autystyczną. W artykule zwrócono również uwagę na wzrastającą ilość powiadomień w ramach europejskiego Systemu Wczesnego Ostrzegania o Niebezpiecznej Żywności i Paszach (Rapid Alert System for Food and Feed –RASFF), dotyczących zanieczyszczenia rtęcią ryb i produktów rybnych. Omówiono także regulacje prawne dotyczące maksymalnych dopuszczalnych poziomów rtęci w żywności.
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