Let R be a prime ring of characteristic different from 2, Qr its right Martindale quotient ring and C its extended centroid. Suppose that F, G are generalized skew derivations of R with the same associated automorphism α, and p(x1, ..., xn) is a non-central polynomial over C such that \left[ {F(x),\alpha (y)} \right] = G(\left[ {x,y} \right]). for all x,y\in \left \{ p\left ( r_{1},...,r_{n} \right ):r_{1},...,r_{n}\in R\right \}. The there exist \lambda \in C such that F(x) = G(x) = λα(x) for all X\in R., Vincenzo De Filippis., and Obsahuje seznam literatury
Autonomic nervous system (ANS) disorders are common in multiple sclerosis (MS). Previous studies showed differences in insulin resistance (IR) and lipoprotein levels in MS subjects compared to controls. Lipolysis caused by increased sympathetic activity could be one of the possible linking mechanisms leading to dyslipidemia in MS. Our study aimed to evaluate ANS activity in the context of glucose and lipid metabolism in people with MS. We prospectively measured short-term heart rate variability (HRV), fasting lipoprotein concentrations, and calculated IR indices based on plasma glucose and insulin levels during oral glucose tolerance test (oGTT) in 32 patients with MS and 29 healthy controls matched for age, sex and body mass index in our study. There was no significant difference in HRV parameters and lipoprotein levels between MS and controls. A significant positive correlation was found between low/high-frequency power ratio (LF/HF) and triglycerides (r=0.413, p=0.021) in MS subjects but not in controls. A significantly lower whole-body insulin sensitivity index (ISIMat) was found in patients with MS compared to the control group (7.3±3.7 vs. 9.8±5.6, p=0.041). No significant correlations were found between LF/HF and IR parameters. In MS subjects, the positive correlation of LF/HF with triglycerides could reflect the effects of sympathetic activity on lipolysis. Positive correlations of sympathetic activity with increased lipoprotein levels could rather reflect processes associated with immune system activation/inflammation, than processes involved in glucose homeostasis maintenance.
A fuzzy model based on an enhanced supervised fuzzy clustering algorithm is presented in this paper. The supervised fuzzy clustering algorithm [6] allows each rule to represent more than one output with different probabilities for each output. This algorithm implements k-means to initialize the fuzzy model. However, the main drawbacks of this approach are that the number of clusters is unknown and the initial positions of clusters are randomly generated. In this work, the initialization is done by the global k-means algorithm [1], which can autonomously determine the actual number of clusters needed and give a deterministic clustering result. In addition, the fast global k-means algorithm [1] is presented to improve the computation time. The model is tested on medical diagnosis benchmark data and Westland vibration data. The results obtained show that the model that uses the global k-means clustering algorithm [1] has higher accuracy when compared to a model that uses the k-means clustering algorithm. Besides that, the fast global k-means algorithm [1] also improved the computation time without degrading much the model performance.
We present data supporting the hypothesis that the lysosomalautophagy pathway is involved in the degradation of intracellular triacylglycerols in the liver. In primary hepatocytes cultivated in the absence of exogenous fatty acids (FFA), both inhibition of autophagy flux (asparagine) or lysosomal activity (chloroquine) decreased secretion of VLDL (very low density lipoproteins) and formation of FFA oxidative products while the stimulation of autophagy by rapamycine increased some of these parameters. Effect of rapamycine was completely abolished by inactivation of lysosomes. Similarly, when autophagic activity was influenced by cultivating the hepatocytes in “starving” (amino-acid poor medium) or “fed” (serum-supplemented medium) conditions, VLDL secretion and FFA oxidation mirrored the changes in autophagy being higher in starvation and lower in fed state. Autophagy inhibition as well as lysosomal inactivation depressed FFA and DAG (diacylglycerol) formation in liver slices in vitro. In vivo, intensity of lysosomal lipid degradation depends on the formation of autophagolysosomes, i.e. structures bringing the substrate for degradation and lysosomal enzymes into contact. We demonstrated that lysosomal lipase (LAL) activity in liver autophagolysosomal fraction was up-regulated in fasting and down-regulated in fed state together with the increased translocation of LAL and LAMP2 proteins from lysosomal pool to this fraction. Changes in autophagy intensity (LC3-II/LC3-I ratio) followed a similar pattern., V. Škop ... [et al.]., and Obsahuje seznam literatury