The transverse (t-) tubular system serves to bring electrical signals deep inside the muscle cells to control mechanical responses. Our preliminary mathematical model of human ventricular cardiomyocyte incorporating t-tubular system [1] was improved by introducing description of latest experimental data related to morphology of human t-tubules and to specific properties of ionic currents. To describe the ion diffusion within t-tubular lumen, we partitioned the t-tubule compartment into nine concentric cylindrical segments. Using the model, we studied the effect of activity-induced concentration changes in the t-tubules on Ca2+ entry into the cell and the intracellular Ca2+ transients controlling the strength of cellular contraction. The values of some crucial parameters, unknown in human cardiomyocytes to date, were regarded as independent variables. The simulations confirmed the tendency of the activity-induced t-tubular concentration changes of Ca2+ to reduce the Ca2+ entry into the cell as well as the intracellular Ca2+ transient. The effect rose with the increase of t-tubular fraction of L-type Ca2+ channels (fCa,t), with the decrease of t-tubular fraction of Ca2+ pump (fpCa,t) and with the increase of the time constant of Ca2+ exchange between external space and t-tubule lumen (TCa,extt). Significant effect simultaneously fCa,t ≥ 0.64, fpCa,t ≤ 0.2 and TCa,extt ≥ 240 ms. and Obsahuje Appendix se seznamy literatury, užitých zkratek a symbolů
In this paper it is proved that every $3$-connected planar graph contains a path on $3$ vertices each of which is of degree at most $15$ and a path on $4$ vertices each of which has degree at most $23$. Analogous results are stated for $3$-connected planar graphs of minimum degree $4$ and $5$. Moreover, for every pair of integers $n\ge 3$, $ k\ge 4$ there is a $2$-connected planar graph such that every path on $n$ vertices in it has a vertex of degree $k$.
To investigate the effect of vanadyl trehalose (VT) on oxidative stress and reduced glutathione/glutathione-Stransferase（GSH/GSTs）pathway gene expression in mouse gastrointestinal tract, as well as the protective effects of vitamin C (VC) and reduced glutathione (GSH). Thirty male Kunming mice were randomly divided into five groups: control group (group A), VT group (group B), VC + VT group (group C), GSH + VT group (group D) and VC + GSH + VT group (group E). The content of reduced glutathione (GSH) and glutathione peroxidase (GSH-Px) activity and the expressions of glutamatecysteine ligase catalytic subunit (GCLC), glutathione synthetase (GSS), regulated through glutathione reductase (GSR) and glutathione-S-transferase pi (GSTpi) in stomach and duodenum in vanadyl trehalose treated group were lower than those in group A (P<0.05). The C, D, E group can significantly improve the above indicators, but those only in the stomach in E group reached the level of the control group. Vanadyl trehalose (VT) was able to cause oxidative stress damage to the gastrointestinal tract of mice, which affects GSH content and GSH-Px activity and interferes with the normal expression of GSH/GSTs pathway. Exogenous vitamin C, reduced glutathione and the combination of the two could play a specific role in antioxidant protection and reduce the toxicity of vanadyl trehalose.
Cadmium is a heavy metal causing toxicity especially in kidney
cells. The toxicity is linked also with enhanced oxidative stress
leading to cell death. On the other hand, our recent experiments
have shown that an increase of total intracellular dehydrogenases
activity can also occur in kidney cells before declining until cell
death. The aim of the present study, therefore, was to evaluate
this transient enhancement in cell viability after cadmium
treatment. The human kidney HK-2 cell line was treated with
CdCl2 at concentrations 0-200 µM for 2-24 h and intracellular
dehydrogenase activity was tested. In addition, we measured
reactive oxygen species (ROS) production, glutathione levels,
mitochondrial membrane potential, and C-Jun-N-terminal kinase
(JNK) activation. We found that significantly increased
dehydrogenase activity could occur in cells treated with 25, 100,
and 200 µM CdCl2. Moreover, the results showed an increase in
ROS production linked with JNK activation following the
enhancement of dehydrogenase activity. Other tests detected
no relationship with the increased in intracellular dehydrogenase
activity. Hence, the transient increase in dehydrogenase activity
in HK-2 cells preceded the enhancement of ROS production and
our finding provides new evidence in cadmium kidney toxicity.