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1

Changing the fate. Results coming from epileptogenesis in tuberous sclerosis

100%
Jozwiak S.
Acta Neurobiologiae Experimentalis
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2017
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tom 77
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nr Suppl.1
Tuberous sclerosis (TS) is a multisystem, genetic, neurocutaneous disorder associated with the development of benign tumours in several organs. Epilepsy affects 70–90% of patients. In the majority of patients epilepsy manifests in the first months of life and half of patients develop cognitive impairment, autism spectrum disorders or other neurodevelopmental disturbances. Our previous studies demonstrated that antiepileptic treatment before the onset of seizures but after electroencephalographic (EEG) deterioration results in significant decrease of clinical seizures, the risk of drug-resistant epilepsy, and relevant improvement in neurodevelopmental outcome. As recently shown the development of epilepsy is a long process called epileptogenesis. Seizures are usually preceded by changes in genes expression, neuronal death, activation of inflammation, finally by changes in the EEG recordings. Intervention at this „latent” stage of epileptogenesis may change the fate of the TS children. The EPISTOP project (Full title: Long-term, prospective study evaluating clinical and molecular biomarkers of epileptogenesis in a genetic model of epilepsy – Tuberous sclerosis complex; www.Epistop.eu) is a multi-center prospective European study tracking epileptogenesis and epilepsy in infants with TS. These studies will allow for the further identification of clinical, molecular and genetic biomarkers that may be used to identify at-risk patients. In the presentation the concept of preventative intervention in epileptogenesis will be discussed. FINANCIAL SUPPORT: We are grateful to all the partners of the EPISTOP consortium who participate in this multi-center European project. Part of the research leading to these results was funded by the European Community’s Seventh Framework Programme (FP7/2007–2013) under grant agreement n°602391 – EPISTOP.
2

Molecular biomarkers of epileptogenesis in a genetic model of epilepsy - tuberus sclerosis complex

100%
Jozwiak S.
Acta Neurobiologiae Experimentalis
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2019
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tom 79
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nr Suppl.1
The aim of EPISTOP was to better understand the pathophysiology of epilepsy and its consequences, to develop a preventative strategy for epilepsy, to identify new biomarkers of epilepsy, and to develop new therapeutic targets to block or otherwise modify epileptogenesis in humans. This aim was achieved by a multidisciplinary, systematic approach. First, a prospective study of epilepsy development was conducted in infants with tuberus sclerosis complex (TSC), using a wide range of clinical, neuroimaging, and genetic analyses, including a diverse set of cutting edge analyses of blood samples, at the onset of epileptiform discharges on EEG, at seizure onset and at the age of 24 month. Second, we performed an analysis of biomarkers of epileptogenesis and drug-resistant epilepsy in epileptogenic brain specimens obtained from patients with TSC who underwent epilepsy surgery and TSC autopsy cases collected in the past.
3
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Wyniki leczenia glistnicy i ancylostomatozy Levo-Tetramizolem-Janssen

51%
Kuzmicki R., Gajda-Kazikowa E., Jozwiak S.
Wiadomości Parazytologiczne
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1972
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tom 18
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nr 1
4

Cell size and proliferation of subependymal giant cell astrocytomas are regulation by mTOR ans Ras-ERK signaling pathway

51%
Tyburczy M., Kotulska K., Jozwiak S., Kaminska B.
Acta Neurobiologiae Experimentalis
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2009
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tom 69
|
nr 3
Tuberous sclerosis complex (TSC) is characterized by cortical developmental malformations that are associated with epilepsy and appearance of benign brain tumors – subependymal giant cell astrocytomas (SEGAs) which are composed of distinct cell types, including giant cells and dysplastic neurons. TSC results from mutations in TSC1 and TSC2, which lead to the mTOR pathway activation, and p70S6 kinase and ribosomal S6 protein phosphorylation. ERK pathway is also aberrantly activated in SEGAs. Clinical trials with the mTOR inhibitor – rapamycin have demonstrated reduction in size of SEGAs, but the molecular mechanisms are unknown. In the present study, we evaluated the effects of rapamycin and the ERK pathway inhibitor – UO126 on cell size, proliferation and viability of cell cultures derived from SEGA. Rapamycin or UO126 alone did not affect viability and proliferation of SEGA cells. However, treatment with both drugs reduced proliferation of SEGA cells. Staining of F-actin revealed decrease of cell size in SEGA cultures exposed to rapamycin alone or in combination with UO126, but treatment with UO126 alone did not infl uence cell size nor morphology. Our studies demonstrate that simultaneous inhibition of both mTOR and ERK signaling pathways reduces proliferation of SEGA cells. Moreover, inhibition of mTOR signaling with rapamycin diminishes a volume of giant SEGA cells. It implicates that inhibitors of mTOR and ERK pathways should be considered for clinical trials of SEGAs.
5

Niezwykła białogłowa

32%
Jozwiak S.
Brać Łowiecka
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2015
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nr 07
6

MRI-monitored cord blood-derived cell transplantation to the ventricular system of child with global cerebral ischemia-a case report

27%
Janowski M., Kmiec T., Jurkiewicz E., Kropiwnicki T., Habich A., Kotulska K., Jelonek E., Sarnowska A., Litwin M., Boruczkowski D., Lukomska B., Walecki J., Roszkowski M., Jozwiak S., Domanska-Janik K.
Acta Neurobiologiae Experimentalis
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2011
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tom 71
|
nr 1
Introduction: Neurological disorders are the most common cause of serious disability and have a major impact on financial healthrelated burden to society. Most of them are definitely associated with cell death: sudden or chronic. Conventional treatment methods yield disappointing results. Thus the discoveries in stem cell biology have fueled the interest in cell-based therapeutical approach. Based on experimental data cord blood has been proposed as a novel, autologous cell source for pediatric population. Non-invasive monitoring of cell fate following transplantation has been recently recommended as a basis for rational stem cell therapy. Subject: One year old child experienced devastating, cardiac arrest-induced cerebral ischemia. Despite a broad rehabilitation program diagnose of vegetative state has been established three months later. After next three months of continued rehabilitation no noticeable improvement has also been found and the child has been included into study. The protocol has been approved by the ethical commission of The Children’s Memorial Health Institute in Warsaw, Poland. Then the child’s own cord blood cells have been neurally-converted over 10 days in culture within GMP facility. Prior to transplantation cells were labeled with iron oxide (SPIO) for MR imaging. For scaling sensitivity of MR signal different concentrations of SPIO-labeled cells were scanned in the phantom. Then patient received monthly 3 subsequent cell infusions (1.2 x 107 cells each) to lateral ventricles. The follow up continued up to 6 months and included both clinical assessment and MR examinations. Results: High efficiency of neural cell conversion and SPIO labeling as well as no cytotoxicity were observed. The employed method of cell transplantation was found to be efficient to deliver cells to CNS as confirmed by MR imaging. Gradual decrease of SPIO signal intensity was observed over the period of follow up. No adverse events or abnormal reaction to cell implantation was detected. The follow up revealed mild functional improvement - decreased nystagmus, spasticity and the number of epileptic seizures. Moreover, the features of the child contact with parents has appeared, thus vegetative state can not be diagnosed any more. Conclusions: This report indicates that transplantation of autologous, neurally-committed cord blood-derived cells to the ventricular system of child is safe, feasible and able to result with mild functional improvement. Additionally cell-related MRI signal can be monitored for more than 4 months in transplanted brain hemisphere. Supported by MSHE grants no 0141/B/P01/2008/35 and 0142/B/ P01/2008/35.
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