Wyniki wyszukiwania - Biblioteka Nauki

1

Patomechanizmy i diagnostyka laboratoryjna choroby Alzheimera

100%

Szutowicz A.

Diagnostyka Laboratoryjna

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2007

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tom 43

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nr 3

2

Interactions of early and late neurotoxic signals in cholinergic neurodegeneration

100%

Szutowicz A.

Acta Neurobiologiae Experimentalis

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2017

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tom 77

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nr Suppl.1

EN

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

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

100%

Szutowicz A.

Diagnostyka Laboratoryjna

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2015

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tom 51

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nr 3

4

Patomechanizmy i diagnostyka laboratoryjna choroby Alzheimera

100%

Szutowicz A.

Diagnostyka Laboratoryjna

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1999

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tom 35

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nr 1

5

Biochemia kliniczna chorób psychicznych

89%

Szutowicz A. , Szutowicz A.

Diagnostyka Laboratoryjna

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1985

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tom 21

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nr 4-5

6

Wspomnienie

88%

Szutowicz A.

Diagnostyka Laboratoryjna

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2013

|

tom 49

|

nr 4

7

Synteza acetylocholiny w synaptosomach

88%

Szutowicz A.

Postępy Biochemii

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1979

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tom 25

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nr 1

8

Encefalopatie otępienne - wczesne i przewlekłe sygnały neurodegeneracyjne

75%

Szutowicz A.

Diagnostyka Laboratoryjna

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2017

|

tom 53

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nr 1A

9

Diagnostyka laboratoryjna - stan obecny, potrzeby i perspektywy rozwoju

63%

Rogulski J. , Szutowicz A.

Diagnostyka Laboratoryjna i Wiadomości PTDL

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1994

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tom 30

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nr 4

10

Regulation of ATP citrate lyase activity in vitro

63%

Szutowicz A. , Angielski S.

Acta Biochimica Polonica

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1970

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tom 17

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nr 3

11

Potrzeby aparaturowe niezbędne dla poprawy stanu diagnostyki laboratoryjnej

63%

Rogulski J. , Szutowicz A.

Diagnostyka Laboratoryjna i Wiadomości PTDL

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1994

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tom 30

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nr 4

12

Acetyl-CoA and acetylcholine metabolism in brain compartments of thiamine-deficient rats

51%

Kisielevski Y. , Tomaszewicz M. , Jankowska A. , Szutowicz A.

Acta Neurobiologiae Experimentalis

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1995

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tom 55

|

nr 5

13

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

51%

Szutowicz A. , Bielarczyk H. , Tomaszewicz M.

Acta Neurobiologiae Experimentalis

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1992

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tom 52

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nr 3

14

The modification of blood platelets activity and the availability of acetyl-CoA in response to hyperglycemia in the course of diabetes

51%

Michno A. , Skibowska A. , Raszeja-Specht A. , Szutowicz A.

Acta Biochimica Polonica

|

2003

|

tom 50

|

nr Supplement 1

15

Toksyczne i niedoborowe uszkodzenia układu cholinergicznego mózgu

51%

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

Diagnostyka Laboratoryjna i Wiadomości PTDL

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1996

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tom 32

|

nr 3

16

Fluorymetryczna metoda oznaczanie wewnątrzkomórkowego cynku z użyciem barwnika TSQ

51%

Dys A. , Szutowicz A. , Bielarczyk H.

Diagnostyka Laboratoryjna

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2017

|

tom 53

|

nr 1A

17

Effect of (-)Hydroxycitrate on the activities of ATP citrate lyase and the enzymes of acetyl-CoA metabolism in rat brain

51%

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

Acta Biochimica Polonica

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1976

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tom 23

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nr 2-3

18

Determination of citrate and CoA by ATP : citrate oxaloacetatel-lyase

51%

Szutowicz A. , Angielski S. , Wojcikowski C.

Acta Biochimica Polonica

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1972

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tom 19

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nr 3

19

Effect of L-carnitine on activities of acetylcoa metabolizing enzymes in SN56 cholinergic septal hybrid cells

51%

Madziar B. , Tomaszewicz M. , Jankowska A. , Szutowicz A.

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nr 3

20

Paracrine interactions between non-activated N9 microglial cells in co-culture with SN56 cholinergic neuronal cells

51%

Gul-Hinc S. , Ronowska A. , Bielarczyk H. , Szutowicz A.

Acta Neurobiologiae Experimentalis

|

2013

|

tom 73

|

nr 1

EN

Microglial cells, through the proinflammatory mediators play an important role in host defense and tissue repair in CNS. They contribute to pathomechanisms of Alzheimer’s and other neurodegenerative diseases. The aim of this work was to investigate modifying effects of non-activated migroglia on cholinergic neuronal SN56 cells subjected to common neuroprotective and/or neurotoxic signals. Chronic exposure to Zn or SNP caused loss of viability (30%), inhibition of pyruvate dehydrogenase (PDH) (40%), isocitrate dehydrogenase (60 and 50%) and aconitase activities as well as decrease of acetyl-CoA levels. These alterations in enzyme activities displayed strong direct correlation with depletion of acetylCoA (r=0.86, P<0.0001) and inverse correlation with cell viability (r=0.87, P<0.0001). Resveratrol, free radical scavenger, increased viability of Zn/SNP treated cholinergic cells but did not overcome suppresive effects of SNP and Zn on enzymes activities. Under same neurotoxic conditions, N9 microglial cells cultured on isoporated inserts and added to neuronal culture dishes, also overcame neurotoxic effect Zn and SNP maintaining control levels of acetyl-CoA, enzymes activites and high cell viability. These data sugest that in some specific, pathologic conditions, non-activated microglia may protect neuronal cholinergic neurons against neurotoxic insults by paracrine-like mechanism by protecting their energy metabolism. On the other hand resveratrol neuroprotection may depend on entirely different yet undefined mechanism. Supported by GUMed MN-15, MNiSW NN401029937, IP2010035370, GUMed ST-57 projects.