Wyniki wyszukiwania

1

Patomechanizmy i diagnostyka laboratoryjna choroby Alzheimera

100%

Szutowicz A.

Diagnostyka Laboratoryjna

|

1999

|

tom 35

|

nr 1

2

Interactions of early and late neurotoxic signals in cholinergic neurodegeneration

100%

Szutowicz A.

Acta Neurobiologiae Experimentalis

|

2017

|

tom 77

|

nr Suppl.1

The loss of neurons and suppression of energy metabolism, in pathology‑affected areas of the brain, are characteristic features of several neurodegenerative conditions including Alzheimer’s disease, and vascular, dialysis, alcohol, liver, or thiamine deficiency encephalopathies. Multiple acute neurotoxic insults such as transient hypoxia, hypoglycemia, or xenobiotics generating excess of free radicals, glutamate-Zn excitotoxic stimulation, trace metal dis-homeostasis, inhibition of energy metabolism, may pave the path for subsequent stages of neurodegeneration. This presentation basing on cellular, animal models of neurotoxicity and clinical-laboratory medicine data, describes putative mechanisms linking early pathological alterations in energy‑acetyl‑CoA metabolism with late stages of different cholinergic encephalopathies. Preferential impairment of basal forebrain cholinergic neurons is blamed for appearance of cognitive deficits leading to dementia in final stages of these pathologies. This phenomenon may result from the fact that cholinergic neurons, unlike other ones utilize a direct key energy precursor metabolite – acetyl-CoA, de rived from glucose, not only for ATP and N-acetylaspartate synthesis but also for acetylcholine production. Cholinergic neurons also possess greater than noncholinergic ones and glial cells zinc accumulation capacity. Such properties promote amyloidogenesis and processing of amyloid‑β precursor protein, yielding accumulation of neurotoxic amyloid‑β[1‑42] oligomers. They may aggravate primary neurotoxic signals through interactions with extracellular and intracellular membranes and linked signal transduction [pathways. Amyloid‑β exerted no direct inhibitory effects on pyruvate dehydrogenase and other enzymes of energy and ACh metabolism. These data indicate that several cytotoxic insults may focus on acetyl-Co-A metabolism as an ultimate target linked with consecutive stages of cholinergic neurodegeneration. FINANCIAL SUPPORT: Supported by St-57 fund Medical University of Gdansk.

3

Patomechanizmy i diagnostyka laboratoryjna choroby Alzheimera

100%

Szutowicz A.

Diagnostyka Laboratoryjna

|

2007

|

tom 43

|

nr 3

4

Hiperglikacja białek wewnątrz i zewnątrzkomórkowych; marker czy aktywny element patomechanizmów cukrzycy

100%

Szutowicz A.

Diagnostyka Laboratoryjna

|

2015

|

tom 51

|

nr 3

5

Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik

Biochemia kliniczna chorób psychicznych

89%

Szutowicz A., Szutowicz A.

Diagnostyka Laboratoryjna

|

1985

|

tom 21

|

nr 4-5

6

Synteza acetylocholiny w synaptosomach

88%

Szutowicz A.

Postępy Biochemii

|

1979

|

tom 25

|

nr 1

7

Wspomnienie

88%

Szutowicz A.

Diagnostyka Laboratoryjna

|

2013

|

tom 49

|

nr 4

8

Encefalopatie otępienne - wczesne i przewlekłe sygnały neurodegeneracyjne

75%

Szutowicz A.

Diagnostyka Laboratoryjna

|

2017

|

tom 53

|

nr 1A

9

Diagnostyka laboratoryjna - stan obecny, potrzeby i perspektywy rozwoju

63%

Rogulski J., Szutowicz A.

Diagnostyka Laboratoryjna i Wiadomości PTDL

|

1994

|

tom 30

|

nr 4

10

Potrzeby aparaturowe niezbędne dla poprawy stanu diagnostyki laboratoryjnej

63%

Rogulski J., Szutowicz A.

Diagnostyka Laboratoryjna i Wiadomości PTDL

|

1994

|

tom 30

|

nr 4

11

Regulation of ATP citrate lyase activity in vitro

63%

Szutowicz A., Angielski S.

Acta Biochimica Polonica

|

1970

|

tom 17

|

nr 3

12

Toksyczne i niedoborowe uszkodzenia układu cholinergicznego mózgu

51%

Szutowicz A., Bilarczyk H., Jankowska A., Tomaszewicz M.

Diagnostyka Laboratoryjna i Wiadomości PTDL

|

1996

|

tom 32

|

nr 3

13

Effect of bicarbonate buffer on the activity of cytoplasmic and mitochondrial alanine aminotransferase

51%

Lysiak W., Pienkowska-Vogel M., Szutowicz A., Angielski S.

Acta Biochimica Polonica

|

1975

|

tom 22

|

nr 3

14

Fluorymetryczna metoda oznaczanie wewnątrzkomórkowego cynku z użyciem barwnika TSQ

51%

Dys A., Szutowicz A., Bielarczyk H.

Diagnostyka Laboratoryjna

|

2017

|

tom 53

|

nr 1A

15

EB12 knock-out mice show greater loss of brain lipids followed by earlier attempts at remyelination in the cuprizone model of demyelination

51%

Klimaszewska-Lata J., Shimshek D. R., Szutowicz A., Rutkowska A.

Acta Neurobiologiae Experimentalis

|

2019

|

tom 79

|

nr Suppl.1

INTRODUCTION: The EBI2 receptor is one of the key mediators of innate immune responses. In cooperation with its ligand, oxysterol 7α,25HC, EBI2 coordinates immune cell positioning in the secondary lymphoid tissue, enabling appropriate humoral and cellular immune responses. EBI2 is also expressed in the central nervous system (CNS), where it regulates inflammatory signalling and myelination. Importantly, EBI2 receptor’s altered expression and signalling have been linked to a range of diseases including multiple sclerosis. AIM(S): The aim of the study was to investigate the effects of EBI2 signalling on lipid parameters in the cuprizone model of demyelination. METHOD(S): 37-week-old EBI2 knock-out (KO) and wild‑type C57BL6J mice were fed a 0.2% cuprizone diet for 5 weeks. The animals were decapitated immediately after 5 weeks or after an additional 2 weeks of recovery period on normal diet. Here, we report greater loss of brain cholesterol and triglycerides in EBI2 KO mice after 5 weeks on the cuprizone diet, indicating EBI2 receptor involvement in CNS lipid maintenance under demyelinating conditions. RESULTS: However, two weeks after return to normal diet, when spontaneous remyelination is observed, the data showed higher cholesterol and triglycerides levels and a greater increase in lipase activity in the EBI2 KO mice. Other studies showed that a sharp increase in lipase activity is observed in an experimental autoimmune encephalomyelitis model around the time of symptom remission and in cerebellar slices between deand re‑myelination phases. CONCLUSIONS: Our data is, therefore, in line with these findings showing that earlier lipase activity in the EBI2 KO mice possibly leads to an earlier remyelination attempt, as observed by increased cholesterol and triglycerides levels. These results indicate functional involvement of EBI2 receptor in lipid homeostasis under pathophysiological conditions and thus warrant further investigations into the role of EBI2 in demyelinating diseases.

16

Kolorymetryczna metody oznaczania aktywności oksydazy monoaminowej w błonach płytek krwi

51%

Szutowicz A., Tomaszewicz M., Orsulak P. J., Ciszek B.

Diagnostyka Laboratoryjna

|

1988

|

tom 24

|

nr 2

17

Modification of acetyl-CoA and ACh metabolism in nerve terminals by dichloroacetate

51%

Szutowicz A., Bielarczyk H., Tomaszewicz M.

Acta Neurobiologiae Experimentalis

|

1992

|

tom 52

|

nr 3

18

Blood platelets as a model for changes of acetyl-CoA metabolism in diabetic brain

51%

Tomaszewicz M., Nowacka M., Skibowska A., Szutowicz A.

Acta Neurobiologiae Experimentalis

|

1999

|

tom 59

|

nr 3

19

Relationships between acetyl-CoA level and function of fenotypically modified N9 murine microglial cells

51%

Klimaszewska-Lata J., Ronowska A., Bielarczyk H., Szutowicz A.

Acta Neurobiologiae Experimentalis

|

2009

|

tom 69

|

nr 1

Neurodegenerative lesions in cholinergic encephalopathies include an excessive activation of microglia, which may aggravate this process. Infl amatory cytokines were reported to affect viability of cultured cholinergic cells, through the infl uence on their acetyl-CoA metabolism. The aim of this work was to investigate whether phenotypic modifi cations of N9 microglia by common neuron-differentiating stimuli can alter its energy metabolism, viability and biological activity in neurodegenerative conditions. In basal conditions lipopolysaccharide (LPS) slightly decreased PDH activity and acetyl-CoA content and activated NO synthesis (600%). The cyclic AMP alone (0.25 mM), caused 15% increase of nonviable cells at 300% rise in NO synthesis and 50 and 30% decreases in acetyl-CoA and ATP contents, respectively. In such conditions LPS resulted in further increase of NO accumulation and aggravated loss of cell viability and their acetyl-CoA content. In basic conditions retinoic acid (RA) alone did not alter viability and NO synthesizing capacity but increased acetyl-CoA and blunted cytotoxic potencies of cAMP and LPS to N9. RA-evoked restoration of N9 cell viability was accompanied by the increase in their acetyl-CoA content. These data indicate that activation of microglia depletes their acetyl-CoA, making them more vulnerable to cytotoxic insults. On the contrary, rescue of microglia by RA-signaling pathways is connected with restoration their acetylCoA pool. Supported by MNiSW projects P05A 11030 and NN401 2333 33 and AMG fund St-57.

20

The activity of ATP citrate lyase in rat brain and liver under various physiological conditions

51%

Szutowicz A., Stepien M., Lysiak W., Angielski S.

Acta Biochimica Polonica

|

1974

|

tom 21

|

nr 3

Ograniczanie wyników

Patomechanizmy i diagnostyka laboratoryjna choroby Alzheimera

Interactions of early and late neurotoxic signals in cholinergic neurodegeneration

Patomechanizmy i diagnostyka laboratoryjna choroby Alzheimera

Hiperglikacja białek wewnątrz i zewnątrzkomórkowych; marker czy aktywny element patomechanizmów cukrzycy

Biochemia kliniczna chorób psychicznych

Synteza acetylocholiny w synaptosomach

Wspomnienie

Encefalopatie otępienne - wczesne i przewlekłe sygnały neurodegeneracyjne

Diagnostyka laboratoryjna - stan obecny, potrzeby i perspektywy rozwoju

Potrzeby aparaturowe niezbędne dla poprawy stanu diagnostyki laboratoryjnej

Regulation of ATP citrate lyase activity in vitro

Toksyczne i niedoborowe uszkodzenia układu cholinergicznego mózgu

Effect of bicarbonate buffer on the activity of cytoplasmic and mitochondrial alanine aminotransferase

Fluorymetryczna metoda oznaczanie wewnątrzkomórkowego cynku z użyciem barwnika TSQ

EB12 knock-out mice show greater loss of brain lipids followed by earlier attempts at remyelination in the cuprizone model of demyelination

Kolorymetryczna metody oznaczania aktywności oksydazy monoaminowej w błonach płytek krwi

Modification of acetyl-CoA and ACh metabolism in nerve terminals by dichloroacetate

Blood platelets as a model for changes of acetyl-CoA metabolism in diabetic brain

Relationships between acetyl-CoA level and function of fenotypically modified N9 murine microglial cells

The activity of ATP citrate lyase in rat brain and liver under various physiological conditions