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Serum Osteocalcin Concentration in Treadmill-Trained Adult Male Wistar Rats

100%
Nowak A., Pogrzebna M., Celichowski J., Pilaczyńska-Szcześniak Ł.
Journal of Human Kinetics
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2008
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vol. 19
121-130
EN
Mechanical stress is considered to be essential for the regulation of bone mass. The purpose of this study was to determine whether treadmill exercise at moderate intensity induces alterations in blood osteocalcin concentration in rats. Male Wistar rats, aged 5 months, were divided randomly into two groups: trained animals (n = 6) and controls (n = 7). Trained rats were exercised 5 days/week for 4 weeks on a motor-driven treadmill. Each exercise session lasted 60 minutes and the average locomotion speed was 16.2 m/min. After completion of the training period, a blood sample was taken for osteocalcin measurement and the hindlimbs medial gastrocnemius muscles were excised and weighed. Comparative analysis showed significantly lower circulating osteocalcin levels in the exercised rats in comparison to control animals. It is possible that the observed decreased blood osteocalcin concentration is transient in nature. Factors including stress may also influenced the results.Serum osteocalcin concentration in treadmill-trained rats
2
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Serum concentration of visfatin is decreased in patients with chronic heart failure

76%
Straburzyńska-Migaj E., Pilaczyńska-Szcześniak Ł., Nowak A., Straburzyńska-Lupa A., Śliwicka E., Grajek S.
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2012
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vol. 59
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issue 3
339-343
EN
Background. There is an increasing interest in the role of adipocytokines in cardiovascular pathophysiology. Aim. The aim of the study was to compare visfatin levels, a novel adipokine, in patients with heart failure (HF) due to the left ventricular systolic dysfunction with those in age- and body mass index (BMI) - matched healthy controls in relation to the parameters of glucose metabolism and high sensitivity C-reactive protein (hsCRP) levels. Material/Subjects and Methods. The study population consisted of 28 males with systolic HF referred for cardiopulmonary exercise testing, divided into two subgroups based on their NYHA class (HF patients NYHAI+II, n=17, and HF patients NYHAIII+IV, n=11), and 23 controls. The following indices were measured in a serum samples: visfatin, hsCRP, glucose and lipid metabolism parameters, and the insulin resistance index HOMAIR (homeostasis model assessment insulin resistance) was calculated. Results. Concentrations of visfatin and high-density lipoprotein cholesterol (HDL-cholesterol) in the HF subjects were significantly lower (p≤0.01) than in controls. The Kruskal-Wallis test showed significant differences between three groups (controls and both subgroups of heart failure patients) in mean levels of visfatin, hsCRP, glucose, HOMAIR and HDL-cholesterol. Conclusion. Serum visfatin concentrations in patients with systolic HF, particularly with more advanced NYHA classes, are significantly lower in comparison to healthy controls and are independent of age or anthropometric and metabolic parameters.
3
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The role of the Amyloid Precursor Protein mutations and PERKdependent signaling pathways in the pathogenesis of Alzheimer’s disease

76%
Rozpędek W., Nowak A., Pytel D., Lewko D., Diehl J. A., Majsterek I.
Acta Universitatis Lodziensis. Folia Biologica et Oecologica
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2016
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vol. 12
48-59
PL
Choroba Alzheimera (ang. Alzheimer’s disease, AD) jest przewlekłą, najczęściej występującą, chorobą neurodegeneracyjną prowadzącą do nieodwracalnych zmian w strukturze, biochemii i funkcjach mózgu. Neurodegeneracja Ośrodkowego Układu Nerwowego (OUN) jest wynikiem odkładania toksycznych złogów amyloidu β (Aβ) w tkance nerwowej mózgu. Rozwój AD jest przyczyną skomplikowanych interakcji między podłożem genetycznym, a czynnikami biologicznymi, które aktywują złożone szlaki molekularne w przebiegu schorzenia. Za jedną z głównych przyczyn uważa się mutacje występujące w genie kodującym Prekursorowe białko amyloidu β (ang. Amyloid beta Precursor Protein, APP) zlokalizowane w pobliżu cięcia białka APP przez wysoce specyficzne sekretazy: α, β oraz γ. Generowanie toksycznej formy Aβ o długości 42-óch aminokwasów, odkładanego w tkance mózgowej jako płytki starcze, zachodzi poprzez drogę amyloidogenną, w której uczestniczą sekretazy β oraz γ. Na podłożu molekularnym główną przyczyną rozwoju choroby AD jest akumulacja błędnie sfałdowanych lub niesfałdowanych białek w lumen Retikulum Plazmatycznego (ang. Endoplasmic Reticulum, ER). Skutkuje to bezpośrednim wywołaniem stresu ER, który prowadzi do aktywacji kinazy PERK, a następnie fosforylacji eukariotycznego czynnika inicjacji translacji 2 (eIF2α). W rezultacie w komórce nerwowej inhibowana jest translacja większości białek oraz dochodzi do preferencyjnej translacji wyłącznie takich białek takich jak ATF4 (ang. Activating Transcriptor 4) oraz, wyniku długotrwałych warunków stresowych, CHOP (ang. CCAAT-enhancer-binding protein homologous protein). Nadekspresja białka CHOP prowadzi do wzmocnienia ekspresji genów kodujących: pro-apoptotyczne białka BH3 domain-only, GADD34 (ang. DNA damage-inducible protein, GADD34 oraz białko o aktywności oksydoreduktazy ER (ang. ER oxidoreductin 1α, ERO1α). W warunkach wysokiego stężenia białka CHOP zostaje osłabiona ekspresja genów kodujących anty-apoptotyczne białka Bcl-2. W rezultacie masa tkanki nerwowej mózgu ulega znaczącemu obniżeniu w wyniku postępującego procesu neurodegeneracji na drodze apoptotycznej śmierć komórkowej w przebiegu AD.
EN
Alzheimer’s disease (AD) is a highly complex, progressive, age-related neurodegenerative human disease entity. The genetic basis of AD is strictly connected with occurrence of mutations in Amyloid Precursor (APP) gene on chromosome 21. Molecular mechanism that leads to AD development still remains unclear. Recent data reported that it is closely correlated with Endoplasmic Reticulum (ER) stress conditions, which subsequently activate Unfolded Protein Response (UPR) signaling pathways, via the induction of protein kinase RNA-like endoplasmic reticulum kinase (PERK), as a self-protective, adaptive response to adverse stress conditions. That results in the attenuation of global protein synthesis and, on the contrary, selective translation of Activating Transcriptor Factor 4 (ATF4) and secretase β. Interestingly, under prolonged, severe ER stress UPR may switch its signal into apoptotic cell death. That ensues by ATF4-CHOP-mediated activation of a range of pro-apoptotic genes and, on the other hand, downregulation of the expression of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) genes. Current investigations suggest that inhibitions of PERK activity may contribute to the attenuation of the deposition of toxic senile plaques in the brain tissue and, as a result, prevent degeneration of neurons and decline in cognitive abilities.
4
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Effects of annual training cycle on the metabolic response to supra-maximal exercise test in beach volleyball players

64%
Pilaczyńska-Szcześniak Ł., Lisiecki D., Kasprzak Z., Karolkiewicz J., Śliwicka E., Nowak A., Podgórski T., Lewandowska M.
Journal of Human Kinetics
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2011
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vol. 27
80-94
EN
The aim of this study was to analyze the effects of sports training on the physiological response to supra-maximal exercise during consecutive phases of the annual training cycle. The study was carried out in volleyball players at the onset of each training phase. VO2 max was determined by an indirect method using the Ästand-Rhyming nomogram and biochemical analyses were performed before and after the Wingate test. Concentrations of lactate in capillary blood were measured and levels of glucose, insulin, visfatin, resistin, thiobarbituric acid reactive substances (TBARS) of serum and the total antioxidative status of plasma were determined using venous blood.Most significant differences with respect to physiological and biochemical variables centered around the pre-competitive phase when compared to other phases of the annual training cycle. Blood visfatin concentration in highly trained volleyball players is reduced by supra-maximal exercise, whereas levels of resistin remain relatively constant at rest. With the exception of the competitive phase, values of the insulin resistance index fit within the reference range. Levels of lipid peroxidation products were inversely correlated with the insulin resistance index and resistin concentrations.The physical training during the annual cycle does not affect resistin levels, but influences insulin, glucose and visfatin concentrations, along with markers of pro-oxidant/antioxidant balance in beach volleyball players.
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