Wyniki wyszukiwania

1

Secondary metabolites from plant cell and tissue cultures

100%

Hoopen H. J. G., Verpoorte R.

Biotechnologia

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1997

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nr 2

2

Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik

The electron transport chain in parasites

100%

Tielens A. G. M., Van Hellemond J. J.

Wiadomości Parazytologiczne

|

1998

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tom 44

|

nr 3

3

The influence of mitochondrial complex I impairment on ROS metabolism under ammonium supply

86%

Podgorska A., Gieczewska K., Rasmusson A., Gardestrom P., Szal B.

BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology

|

2013

|

tom 94

|

nr 2

4

The content of purine nucleotides in the life cycle and winter numbness state in snail Helix aspersa maxima

86%

Rac M., Safranow K., Machoy Z.

Polish Journal of Natural Sciences

|

2002

|

tom 10

5

Brain energy metabolism in neurodegeneration of dopaminergic neurons in animal model of early Parkinson's disease: role of astrocytes

72%

Kuter K., Olech L., Glowacka U., Paleczna M., Kosmowska B., Jurga A.

Acta Neurobiologiae Experimentalis

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2019

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tom 79

|

nr Suppl.1

Glial pathology and energy metabolism changes in the brain precede symptoms of Parkinson’s disease (PD) and multiple other neurodegenerative diseases. Astrocytes govern and regulate a large part of the energy metabolism in the brain. Prolonged impairment of astrocytic functions could increase the vulnerability of dopaminergic neurons in the substantia nigra (SN). In this model, 40‑50% of dopaminergic neurons were selectively killed, causing transient locomotor disability compensated with time. We also induced death of astrocytes in the SN, simultaneously activating microglia but sparing the dopaminergic neurons. The astrocytes replenished after toxin withdrawal. We studied multiple markers of energy metabolism and mitochondrial oxidative phosphorylation (OxPhos) complex and supercomplex functioning during the early stages of neurodegeneration and compensation in the SN and striatum (STR). Death of astrocytes diminished the capability of the dopaminergic system to compensate for the degeneration of neurons. It caused a local energy deprivation, a shift in the usage of energy substrates, via increased glycogenolysis and glycolysis markers, ketone bodies availability, and fatty acid transport in remaining glial cells. Increased neuronal expression of CPT1c and astrocytic expression of CPT1a suggest adaptation in fatty acid use. On the other hand, lesion of dopaminergic neurons influenced OxPhos system and enhanced its functioning. Microglia activation also plays an important role in the processes of degeneration, compensation, and energy metabolism regulation. Modulation of its activation phenotypes might be beneficial towards the indicated processes. Astrocyte and microglia energetic influence is one of the factors in the neuronal compensatory mechanisms of dopaminergic system and might have a leading role in presymptomatic PD stages.

6

Understanding mitotane mode of action

72%

Waszut U., Szyszka P., Dworakowska D.

Journal of Physiology and Pharmacology

|

2017

|

tom 68

|

nr 1

7

Protozoa and oxygen

72%

Fenchel T.

Acta Protozoologica

|

2014

|

tom 53

|

nr 1 Spec.is. Marine Heterotrophic Protists

8

MiRNA - a novel functional component of food?

72%

Wojciechowska K.

Towaroznawcze Problemy Jakości. Polskie Towarzystwo Towaroznawcze

|

2013

|

nr 2

9

Obesity, the pandemic of XXIst century

72%

Racz O., Frantisek N., Dombrovsky P., Jakubowski K., Kuchelova Z., Macekova D., Cimbolakova I., Kuzmova D.

Prace Naukowe Akademii im. Jana Długosza w Częstochowie. Kultura Fizyczna

|

2014

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tom 13

|

nr 1

A comprehensive review about the current situation in obesity and its consequences. The authors in the first parts of the paper define obesity, describe the methods for assessment of obesity and the amount of fat in the body and discuss the question if obesity itself is a disease or not. According to their view obesity is not a disease but a pathological condition caused by a disturbance of appetite regulation, as well as a gateway to many diseases. In the next part they present the most important data about the epidemiology of obesity in the world and in Europe. The consequences of obesity depend on the distribution pattern of the fat in the human body. Upper body obesity associated with visceral accumulation of fat is more dangerous as compared with mild gluteal obesity in young women. The subsequent chapters copmprise a simple overview of the pathogensis of obesity from the point of view of the energy metabolism and the genetic, epigenetic and environmental factors involved in the development of obesity. The consequences of obesity heavily increase health care and indirect economic costs in rich countries. The most important among these are type 2 diabetes mellitus, coronary heart diseas, hypertension, stroke and gout. The treatment of obesity is often a troublesome and frutrating process both for health-care providers and the affected people. Therefore the psychological and social aspects of overeating are of crucial importance to understand obesity and to elaborate successful ways to prevent it.

10

Disorders of purine metabolism in human erythrocytes in the state of lead contamination

72%

Baranowska-Bosiacka I., Hlynczak A. J., Wiszniewska B., Marchlewicz M.

Polish Journal of Environmental Studies

|

2004

|

tom 13

|

nr 5

Although many countries now have programs to lower the levels of lead in the environment, human exposure to Pb remains of concern to public health officials worldwide. The mechanisms of lead toxicity are still not fully understood, but recent findings have recognized the significance of the lead-induced impairment of the cell energy metabolism. This review outlines recent hypotheses and evidence on the role of nucleotide purines in erythrocyte metabolism regulation. It also describes the resynthesis and decomposition of purine nucleotides in erythrocytes, lead distribution in blood and its influence on purine conversion pathways and both glycolytic and pentosophosphate pathway enzymes in erythrocytes.

11

Control of energy metabolism in the heart and endothelial cells

72%

Schrader J., Decking U. K. M., Stumpe T., Culic O.

Cellular and Molecular Biology Letters

|

1999

|

tom 04

|

nr 3

12

The impact of research on parasites beyond parasitology

72%

Kohler P.

Acta Parasitologica

|

2001

|

tom 46

|

nr 1

13

Energy metabolism of Varroa destructor mites and its implication on host vigour

72%

Garedew A., Schmolz E., Schricker B., Polaczek B., Lamprecht I.

Journal of Apicultural Science

|

2002

|

tom 46

|

nr 2

14

Guanine and inosine nucleotides, nucleosides and oxypurines in snail muscles as potential biomarkers of fluoride toxicity

72%

Rac M. E., Safranow K., Dolegowska B., Machoy Z.

Folia Biologica

|

2007

|

tom 55

|

nr 3-4

15

Is lead toxicosis a reflection of altered energy metabolism in brain synaptosomes ?

72%

Rafalowska U., Struzynska L., Dabrowska-Bouta B., Lenkiewicz A.

Acta Neurobiologiae Experimentalis

|

1996

|

tom 56

|

nr 2

16

Energy metabolism in plants under water deficits

72%

Zagdanska B.

Acta Biochimica Polonica

|

1995

|

tom 42

|

nr 3

Regardless of the mechanisms of stress resistance, the maintenance of functional integrity in plants imposes an energetic cost. This mini-review summarized the present knowledge on energy metabolism in plants under drought conditions with the focus on studies performed on wheat in author's laboratory.

17

The effect of ambient temperature on energy metabolism and activity in adult male mink [ Mustela vison ]

72%

Hissink H. H. A. L., Verstegen M. W. A., De Jonge G.

Zeszyty Naukowe. Przegląd Hodowlany

|

1996

|

tom 29

18

The influence of dietary vitamin A supplementation on vitamin A and insulin levels in sedentary or physically trained rats

58%

Debski B., Gralak M., Gronowska-Senger A., Gornicka M.

Polish Journal of Veterinary Sciences

|

2009

|

tom 12

|

nr 4

Male rats of Wistar strain (n = 48) were fed a vitamin A deficient diet for 3 days of adaptation period and then a 10 day experimental period to reduce slightly the body stores of this vitamin. Half of the animals were subjected to physical training and/or oral vitamin A supplementation. Four different doses of supplementation were used – 0, 7.5, 15 and 60 μg/d/rat, which is equivalent to 0, 25, 50 and 200 IU of vitamin A, respectively. Animals from the defined groups ran on a treadmill with a rate of 2.0 m/s for 15 minutes per day for 10 days. After overnight fasting, the rats were sacrificed, and insulin in blood serum and hepatic retinol concentrations were estimated. Daily feed intake and daily body gains were similar in groups of sedentary and physically trained rats. A moderate level of oral vitamin A supplementation (the highest supplemented dose was about 6 x the above recommended NRC level) did not cause any changes in these zootechnical parameters. Oral Vitamin A supplementation resulted in an increase in retinol concentration in the liver (F = 15.2, p < 0.001), but without significant difference between trained and untrained animals. Physical training of rats caused a statistically significant decrease of insulin concentration in blood serum (1.53 ± 0.18 vs. 1.73 ± 0.20). This difference was highly significant (F = 11.1, p < 0.001). Vitamin A supplementation was found not to influence the concentration of this hormone, which is responsible for energy metabolism regulation in the body. Based on estimated parameters, the necessity of vitamin A excessive use in physically trained subjects was not proven.

19

Influence of balance of protein and energy metabolism in rumen on hypomagnesaemia in cows

58%

Gehrke M.

Polish Journal of Veterinary Sciences

|

2005

|

tom 08

|

nr 3

20

Neutrophils-induced increase of adenosine triphosphate depletion in rat neonatal cardiac myocytes with impaired energy metabolism

58%

Gajewski M., Laskowska-Bozek H., Maslinski S., Ryzewski J.

Journal of Physiology and Pharmacology

|

1991

|

tom 42

|

nr 4

Isolated, cultured rat neonatal cardiac myocytes were placed in medium suppled menfed with mitochondrial respiratory inhibitor potassium cyanide which caused a rapid adenosine triphosphate (ATP) depletion. These myocytes with the impaired energy metabolism (“hypoxia-like state”) were exposed to unstimulated human neutrophils. Effect of human neu rophils on the myocy es m the “hypoxia-like state” was quantified as a total change in the amount of ATP in cardiac cells. After 5 hours of incubation of neu rophils with the myocytes in the “hypoxia-like state” an additional decrease (of 50 per cent) in ATP content was observed. Since catalase (which destroys hydrogen peroxide) prevented the further decline in ATP level in the myocy es with impaired energy metabolism, it seem that hydrogen peroxide and possibly their products are responsible for this effect. These results suggest that unstimulated human neu rophils af er activation by the contact with injured cardiac cells caused further decrease of ATP level in target cells.

Ograniczanie wyników

Secondary metabolites from plant cell and tissue cultures

The electron transport chain in parasites

The influence of mitochondrial complex I impairment on ROS metabolism under ammonium supply

The content of purine nucleotides in the life cycle and winter numbness state in snail Helix aspersa maxima

Brain energy metabolism in neurodegeneration of dopaminergic neurons in animal model of early Parkinson's disease: role of astrocytes

Understanding mitotane mode of action

Protozoa and oxygen

MiRNA - a novel functional component of food?

Obesity, the pandemic of XXIst century

Disorders of purine metabolism in human erythrocytes in the state of lead contamination

Control of energy metabolism in the heart and endothelial cells