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Katerina Stambolieva Dorina Petrova Mariya Irikeva 《Somatosensory & motor research》2017,34(2):129-133
Purpose: To evaluate the effectiveness of 8-week low-frequency plantar vibration training on patients with sensorimotor diabetic peripheral neuropathy (DPN).
Participants: Twelve patients took part in the investigation.
Results: An increase of the nerve conductive velocity of soral and peroneal nerves of feet, increased postural stability, and disappearance of the pain and tingling were observed.
Conclusion: The obtained results provide evidence for beneficial effects of 8-week plantar vibration training in patients with DPN. 相似文献
33.
Involvement of oxidative stress and caspase 2-mediated intrinsic pathway signaling in age-related increase in muscle cell apoptosis in mice 总被引:1,自引:1,他引:0
Braga M Sinha Hikim AP Datta S Ferrini MG Brown D Kovacheva EL Gonzalez-Cadavid NF Sinha-Hikim I 《Apoptosis : an international journal on programmed cell death》2008,13(6):822-832
Apoptosis has been implicated as a mechanism of loss of muscle cells in normal aging and plays an important role in age-related
sarcopenia. To test the hypothesis that caspase 2 and c-Jun NH2-terminal kinase (JNK)-mediated intrinsic pathway signaling contribute to skeletal muscle cell apoptosis in aging, we compared
activation of caspase 2 and JNK and the in vivo expression of 4-hydroxynonenal protein adducts (4-HNE), inducible nitric oxide
synthase (iNOS), glucose-6-phosphate dehydrogenase (G6PDH), B-cell lymphoma-2 (BCL-2), BAX, and phospho-BCL-2 in gastrocnemius
muscles of young (5 months old) and old (25 months old) mice. A distinct age-related increase in 4-HNE and iNOS expression
was readily detected in mice. Increased oxidative stress and iNOS induction were further accompanied by a decrease in G6PDH
expression, activation of caspase 2 and JNK, and inactivation of BCL-2 through phosphorylation at serine 70, and caspase 9
activation. Regression analysis further revealed that increased muscle cell death in aging was significantly correlated with
changes in the levels of these molecules. Taken together, our data indicate that caspase 2 and JNK-mediated intrinsic pathway
signaling is one of the mechanisms involved in age-related increase in muscle cell apoptosis. 相似文献
34.
Differences between Ca2+ and Mg2+ in DNA binding and release by the SfiI restriction endonuclease: implications for DNA looping
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Stuart R. W. Bellamy Yana S. Kovacheva Ishan Haji Zulkipli Stephen E. Halford 《Nucleic acids research》2009,37(16):5443-5453
Many enzymes acting on DNA require Mg2+ ions not only for catalysis but also to bind DNA. Binding studies often employ Ca2+ as a substitute for Mg2+, to promote DNA binding whilst disallowing catalysis. The SfiI endonuclease requires divalent metal ions to bind DNA but, in contrast to many systems where Ca2+ mimics Mg2+, Ca2+ causes SfiI to bind DNA almost irreversibly. Equilibrium binding by wild-type SfiI cannot be conducted with Mg2+ present as the DNA is cleaved so, to study the effect of Mg2+ on DNA binding, two catalytically-inactive mutants were constructed. The mutants bound DNA in the presence of either Ca2+ or Mg2+ but, unlike wild-type SfiI with Ca2+, the binding was reversible. With both mutants, dissociation was slow with Ca2+ but was in one case much faster with Mg2+. Hence, Ca2+ can affect DNA binding differently from Mg2+. Moreover, SfiI is an archetypal system for DNA looping; on DNA with two recognition sites, it binds to both sites and loops out the intervening DNA. While the dynamics of looping cannot be measured with wild-type SfiI and Ca2+, it becomes accessible with the mutant and Mg2+. 相似文献
35.
Mariya V. Kovaleva Evgeniya I. Sukhanova Tatyana A. Trendeleva Marina V. Zyl’kova Ludmila A. Ural’skaya Kristina M. Popova Nils-Erik L. Saris Renata A. Zvyagilskaya 《Journal of bioenergetics and biomembranes》2009,41(3):239-249
In this study we used tightly-coupled mitochondria from Yarrowia lipolytica and Dipodascus (Endomyces) magnusii yeasts, possessing a respiratory chain with the usual three points of energy conservation. High-amplitude swelling and collapse
of the membrane potential were used as parameters for demonstrating induction of the mitochondrial permeability transition
due to opening of a pore (mPTP). Mitochondria from Y. lipolytica, lacking a natural mitochondrial Ca2+ uptake pathway, and from D. magnusii, harboring a high-capacitive, regulated mitochondrial Ca2+ transport system (Bazhenova et al. J Biol Chem 273:4372–4377, 1998a; Bazhenova et al. Biochim Biophys Acta 1371:96–100, 1998b; Deryabina and Zvyagilskaya Biochemistry (Moscow) 65:1352–1356, 2000; Deryabina et al. J Biol Chem 276:47801–47806, 2001) were very resistant to Ca2+ overload. However, exposure of yeast mitochondria to 50–100 μM Ca2+ in the presence of the Ca2+ ionophore ETH129 induced collapse of the membrane potential, possibly due to activation of the fatty acid-dependent Ca2+/nH+-antiporter, with no classical mPTP induction. The absence of response in yeast mitochondria was not simply due to structural
limitations, since large-amplitude swelling occurred in the presence of alamethicin, a hydrophobic, helical peptide, forming
voltage-sensitive ion channels in lipid membranes. Ca2+- ETH129-induced activation of the Ca2+/H+-antiport system was inhibited and prevented by bovine serum albumin, and partially by inorganic phosphate and ATP. We subjected
yeast mitochondria to other conditions known to induce the permeability transition in animal mitochondria, i.e., Ca2+ overload (in the presence of ETH129) combined with palmitic acid (Mironova et al. J Bioenerg Biomembr 33:319–331, 2001; Sultan and Sokolove Arch Biochem Biophys 386:37–51, 2001), SH-reagents, carboxyatractyloside (an inhibitor of the ADP/ATP translocator), depletion of intramitochondrial adenine nucleotide
pools, deenergization of mitochondria, and shifting to acidic pH values in the presence of high phosphate concentrations.
None of the above-mentioned substances or conditions induced a mPTP-like pore. It is thus evident that the permeability transition
in yeast mitochondria is not coupled with Ca2+ uptake and is differently regulated compared to the mPTP of animal mitochondria. 相似文献
36.
Milan Makwana Tsvetan Serchov† Mariya Hristova Marion Bohatschek reas Gschwendtner‡ Roger Kalla‡ ZhiQiang Liu‡ Rolf Heumann† Genndij Raivich§ 《Journal of neurochemistry》2009,108(6):1453-1463
Activation of Ras into the GTP-binding, 'ON' state is a key switch in the neurotrophin-mediated neuronal survival and neurite outgrowth, in vitro as well as in vivo . In the current study we explored changes in GTP-Ras levels following facial nerve injury and the ensuing regeneration and the effects of perturbing these changes in vivo using synapsin-promoter mediated neuronal expression of constitutively active Val12H-Ras (synRas). Quantification of GTP-Ras and total Ras revealed a precipitous drop in the relative GTP-Ras levels in the axotomized facial motor nucleus, to 40% of normal levels at 2 days after cut, followed by a partial recovery to 50–65% at 4–28 days. On western blots, control and axotomized nuclei from synRas mutants showed a 2.2- and 2.5-fold elevation in GTP-Ras, respectively, compared with their wild type littermate controls ( p < 5%, anova , TUKEY post-hoc ), with the levels in the axotomized synRas nucleus slightly but not significantly above that in the uninjured littermate control ( p = 9.9%). Similar increase was also observed in the pERK but not pAKT targets of the Ras cascade. This moderate elevation of GTP-Ras strongly curtailed post-traumatic neuronal cell death (−65%), the influx of T-cells (−48%) as well as other parameters of neuroinflammatory response. Although synRas did not affect the speed of axonal regeneration or functional recovery it caused a very pronounced increase in central axonal sprouting. These current data emphasize the role of reduced active Ras, and by extension, the reduced overall level of retrograde neurotrophin signalling after axotomy, in mediating post-traumatic cell death and inflammation and in restricting the sprouting response. Moreover, the neuroprotective and central sprouting-enhancing effects of neuronal Val12H-Ras could help promote recovery in CNS injury. 相似文献
37.
Petrova NS Meschaninova MI Venyaminova AG Zenkova MA Vlassov VV Chernolovskaya EL 《FEBS letters》2011,585(14):2352-2356
The thermodynamic properties of siRNA duplexes are important for their silencing activity. siRNAs with high thermodynamic stability of both the central part of the duplex and in the whole, usually display low silencing activity. Destabilization of the central part of the siRNA duplex could increase its silencing activity. However, mismatches located in the central part of the duplex could substantially decrease the amount of RNAi efficacy, hindering active RISC formation and function. In this study, we examined the impact of duplex destabilization by nucleotide substitutions in the central part (7-10 nt counting from the 5'-end of the antisense strand) of the nuclease-resistant siRNA on its silencing activity. 相似文献
38.
Kucherenko MM Marrone AK Rishko VM Magliarelli Hde F Shcherbata HR 《Developmental biology》2011,352(2):1102-242
In Drosophila, like in humans, Dystrophin Glycoprotein Complex (DGC) deficiencies cause a life span shortening disease, associated with muscle dysfunction. We performed the first in vivo genetic interaction screen in ageing dystrophic muscles and identified genes that have not been shown before to have a role in the development of muscular dystrophy and interact with dystrophin and/or dystroglycan. Mutations in many of the found interacting genes cause age-dependent morphological and heat-induced physiological defects in muscles, suggesting their importance in the tissue. Majority of them is phylogenetically conserved and implicated in human disorders, mainly tumors and myopathies. Functionally they can be divided into three main categories: proteins involved in communication between muscle and neuron, and interestingly, in mechanical and cellular stress response pathways. Our data show that stress induces muscle degeneration and accelerates age-dependent muscular dystrophy. Dystrophic muscles are already compromised; and as a consequence they are less adaptive and more sensitive to energetic stress and to changes in the ambient temperature. However, only dystroglycan, but not dystrophin deficiency causes extreme myodegeneration induced by energetic stress suggesting that dystroglycan might be a component of the low-energy pathway and act as a transducer of energetic stress in normal and dystrophic muscles. 相似文献
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Misquitta LV Misquitta Y Cherezov V Slattery O Mohan JM Hart D Zhalnina M Cramer WA Caffrey M 《Structure (London, England : 1993)》2004,12(12):2113-2124
Monoacylglycerols have been used as bilayered hosts for growing crystals of membrane proteins. To date, the lipids used have had chains 16 and 18 carbon atoms long. We hypothesized that a shorter-chained lipid producing a thinner bilayer would facilitate the so-called in meso crystallization process. A 14 carbon monoacylglycerol was chosen as the lipid with which to test the proposal. To be compatible with the in meso method, a cis olefinic bond was placed in its acyl chain at a location arrived at by rational design. The target lipid was synthesized and was shown to form the requisite mesophase at room temperature. In support of the hypothesis, it produced crystals of bacteriorhodopsin and the outer membrane transporter, BtuB. The latter is the first beta barrel protein to be crystallized by the in meso method. Protein stability in the short-chain lipid and how this relates to crystallogenesis are discussed. 相似文献
40.
Andriy S. Yatsenko April K. Marrone Mariya M. Kucherenko Halyna R. Shcherbata 《Journal of visualized experiments : JoVE》2014,(88)
Metabolic disorders are a frequent problem affecting human health. Therefore, understanding the mechanisms that regulate metabolism is a crucial scientific task. Many disease causing genes in humans have a fly homologue, making Drosophila a good model to study signaling pathways involved in the development of different disorders. Additionally, the tractability of Drosophila simplifies genetic screens to aid in identifying novel therapeutic targets that may regulate metabolism. In order to perform such a screen a simple and fast method to identify changes in the metabolic state of flies is necessary. In general, carbon dioxide production is a good indicator of substrate oxidation and energy expenditure providing information about metabolic state. In this protocol we introduce a simple method to measure CO2 output from flies. This technique can potentially aid in the identification of genetic perturbations affecting metabolic rate. 相似文献