Wyniki wyszukiwania - Biblioteka Nauki

1

An ultrastructural study of the myelination of the trigeminal ganglion in human foetuses aged 10 to 23 weeks

100%

Bruska M.

Folia Morphologica

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2003

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tom 62

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nr 3

231-233

EN

An ultrastructural study was performed on trigeminal ganglia removed from foetuses aged 10 to 23 weeks. The first turns of lemmocyte processes around the axons were observed in the trigeminal ganglion in the 12th week of development. During the period between the 15th and the 18th weeks the myelin sheath increases in thickness and becomes a compact, laminated structure. In foetuses of 23 weeks the compact myelin sheath has up to 24 myelin lamellae.

2

Ultrastructural picture of rat cerebellum in culture subjected to the action of antiglial immune serum

72%

Weinrauder H. , Gajkowska B.

Bulletin of the Polish Academy of Sciences. Biological Sciences

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1987

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tom 35

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nr 1-3

3

Automatic segmentation of infant brain MR images: With special reference to myelinated white matter

72%

Devi C. N. , Chandrasekharan A. , Sundararaman V. K. , Alex Z. C.

Biocybernetics and Biomedical Engineering

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2017

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tom Vol. 37, no. 1

143--158

EN

Automatic segmentation of infant brain images is faced with numerous challenges like poor image contrast, motion artifacts, and changes caused by progressive myelination of the infant brain. Since timely myelination points to normal brain maturity, monitoring the progress and degree of myelination is clinically significant. However, most of the existing segmentation methods do not segment myelinated portions of the infant brain. In this paper, we propose a segmentation approach focused on segmenting the myelinated white matter tissue in T1-weighted magnetic resonance images of the infant brain. The novelty of the algorithm lies in the introduction of a weighted localized Tsallis entropy based thresh-olding method. The proposed method is also tested on older babies beyond the one-year age mark to verify its utility and robustness. It is seen that the mean Dice coefficients obtained for myelin segmentation by the proposed weighted localized method are higher than that of the other methods, namely, the conventional Tsallis entropy thresholding and modified localized method.

4

Schwann units in the human foetal phrenic nerve

72%

Bruska M. , Piotrowski A. , Wozniak W.

Folia Morphologica

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2005

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tom 64

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nr 4

253-268

EN

In three human foetuses aged 15, 17, and 23 weeks the number of axons surrounded by single Schwann cells was counted. These Schwann cell/axon complexes form the Schwann units. The largest Schwann units in the foetus aged 15 weeks contained 232 axons, in the foetus of 17 weeks the number was 140 and in the foetus of 23 weeks the largest units contained 65 axons.

5

Fine structure and myelination of the greater splanchnic nerves in human fetuses

72%

Wozniak W. , Bruska M.

Folia Morphologica

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1986

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tom 45

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nr 3

6

Microglial expression of peptidylarginine deiminase 2 in the prenatal rat brain

72%

Asaga H. , Ishigami A.

Cellular and Molecular Biology Letters

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2007

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tom 12

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nr 4

536-544

EN

Peptidylarginine deiminases (PADs) are Ca2t+-dependant post-translational modification enzymes that catalyze the citrullination of protein arginyl residues. PAD type 2 (PAD2) is thought to be involved in some processes of neurodegeneration and myelination in the central nervous system. In this study, we found PAD2-positive cells in rat cerebra in 19-to 21-day old embryos, i.e. at a developmental stage well before myelination begins. Most of the cells were microglial marker-positive cells found mainly in the prospective medulla, and others were microglial marker-negative cells found mainly in the prospective dentate gyrus of the hippocampus. The former seemed to be in an activated state as judged by morphological criteria. The specificity of the enzyme activity, immunoblotting and reverse transcriptase-polymerase chain reaction analyses revealed that these cells expressed PAD2 and not PAD1, PAD3 or PAD4. Our data is indicative of microglial expression of PAD2 in the prenatal developing cerebrum.

7

Progress in myelin formation of the thoracic sympathetic trunk in human fetus aged 17 weeks

72%

Bruska M. , Wozniak W.

Folia Morphologica

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1997

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tom 56

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nr 3

8

The role of oligodendrocytes in chronic pain: cellular and molecular mechanisms

58%

Malta I. , Moraes T. , Rodrigues G. , Franco P. , Galdino G.

Journal of Physiology and Pharmacology

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2019

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tom 70

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nr 5

9

Zaburzenia mielinizacji i migracji neuronalnej w patogenezie schizofrenii - poszukiwanie nowych genów kandydujących

58%

Gawłowska M. , Rabe-Jabłońska J.

Psychiatria i Psychologia Kliniczna

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2007

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tom 7

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nr 2

66-75

EN

According to the neurodevelopmental hypothesis, schizophrenia may be caused by structural defects or abnormal neuronal circuits, resulting from disturbed early stages of embryonal development of the central nervous system. Disorders detected within white matter structures are considered one of possible causes of subsequent development of schizophrenia. Disorganization of white matter in patients with schizophrenia has been confirmed by neuropathological and neuroimaging studies. Novel neuroimaging techniques (diffusion tensor and magnetization transfer MRI) confirm the presence of white matter volume loss and regional misrouting and/or deficits within neuronal tracts. Schizophrenia is associated both with disorganization of oligodendrocytes participating in myelin synthesis and disturbed expression of proteins controlling this process. Results of post-mortem studies provide an indirect proof of disturbed neuronal migration taking place at early stages of neuroembryogenesis in patients with schizophrenia. It is suggested, that structural abnormalities observed may be caused by disturbed function of proteins which control this process, e. g. reelin, or substances mieacting as regulators of activity of these proteins and their receptors. Such a potential regulating factor is the product of the HAR1 gene, which may constitute the next step in the pathogenesis of schizophrenia.

PL

W myśl hipotezy neurorozwojowej u podłoża schizofrenii leżą deficyty strukturalne lub nieprawidłowe obwody neuronalne powstające na skutek zaburzeń wczesnych etapów rozwoju embrionalnego ośrodkowego układu nerwowego. Uważa się, że jedną z możliwych przyczyn rozwoju schizofrenii mogą być nieprawidłowości obserwowane w obrębie struktur istoty białej. Na zaburzoną organizację istoty białej wśród chorujących na schizofrenię wskazują wyniki badań neuropatologicznych i neuroobrazowych. Nowe techniki badań obrazowych (badania rezonansu magnetycznego z zastosowaniem tensora dyfuzji i transferu magnetyzacji) potwierdzają obecność ubytków objętości struktur istoty białej oraz regionalne zaburzenia przebiegu i/lub ubytki w obrębie włókien nerwowych. W schizofrenii stwierdza się zarówno nieprawidłową organizację zaangażowanych w syntezę mieliny oligodendrocytów, jak i zaburzoną ekspresję białek regulujących przebieg tego procesu. Wyniki badań pośmiertnych wskazują pośrednio także na zaburzenia migracji neuronalnej na wczesnych etapach neuroembriogenezy wśród pacjentów chorujących na schizofrenię. Sugeruje się, że u podłoża obserwowanych nieprawidłowości strukturalnych leżą zaburzenia funkcji białek zaangażowanych w kontrolę przebiegu tego procesu, takich jak reelina, lub cząstek działających jako regulatory aktywności tych białek lub ich receptorów. Takim potencjalnym czynnikiem regulacyjnym jest produkt genu HAR1, który może stanowić kolejne ogniwo w patogenezie schizofrenii.