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Structural and functional changes ensue in cardiac cell networks when cells are guided by three-dimensional scaffold topography. We report enhanced synchronous pacemaking activity in association with slow diastolic rise in intracellular Ca2+ concentration ([Ca2+]i) in cell networks grown on microgrooved scaffolds. Topography-driven changes in cardiac electromechanics were characterized by the frequency dependence of [Ca2+]i in syncytial structures formed of ventricular myocytes cultured on microgrooved elastic scaffolds (G). Cells were electrically paced at 0.5-5 Hz, and [Ca2+]i was determined using microscale ratiometric (fura 2) fluorescence. Compared with flat (F) controls, the G networks exhibited elevated diastolic [Ca2+]i at higher frequencies, increased systolic [Ca2+]i across the entire frequency range, and steeper restitution of Ca2+ transient half-width (n = 15 and 7 for G and F, respectively, P < 0.02). Significant differences in the frequency response of force-related parameters were also found, e.g., overall larger total area under the Ca2+ transients and faster adaptation of relaxation time to pacing rate (P < 0.02). Altered [Ca2+]i dynamics were paralleled by higher occurrence of spontaneous Ca2+ release and increased sarcoplasmic reticulum load (P < 0.02), indirectly assessed by caffeine-triggered release. Electromechanical instabilities, i.e., Ca2+ and voltage alternans, were more often observed in G samples. Taken together, these findings 1) represent some of the first functional electromechanical data for this in vitro system and 2) demonstrate direct influence of the microstructure on cardiac function and susceptibility to arrhythmias via Ca(2+)-dependent mechanisms. Overall, our results substantiate the idea of guiding cellular phenotype by cellular microenvironment, e.g., scaffold design in the context of tissue engineering.

Microcystin-LR (MC-LR) and microcystin-RR (MC-RR) are the two most common microcystins (MCs) present in fresh water posing a direct threat to public health because of their hepatotoxicity. A novel MC-degrading bacterium designated MC-LTH1 capable of degrading MC-LR and -RR was isolated, and the degradation rates and mechanisms of MC-LR and -RR for this bacterium were investigated. The bacterium was identified as Bordetella sp. and shown to possess a homologous mlrA gene responsible for degrading MCs. To the best of our knowledge, this is the first report of mlrA gene detection in Bordetella species. MC-LR and -RR were completely degraded separately at rates of 0.31 mg/(L h) and 0.17 mg/(L h). However, the degradation rates of MC-LR and -RR decreased surprisingly to 0.27 mg/(L h) and 0.12 mg/(L h), respectively, when both of them were simultaneously present. Degradation products were identified by high performance liquid chromatography coupled with time-of-flight mass spectrometry. Adda (m/z 332.2215, C20H29NO3) commonly known as a final product of MC degradation by isolated bacteria was detected as an intermediate in this study. Linearized MC-LR (m/z 1013.5638, C49H76N10O13), linearized MC-RR (m/z 1056.4970, C49H77N13O13), and tetrapeptide (m/z 615.3394, C32H46N4O8) were also detected as intermediates. These results indicate that the bacterial strain MC-LTH1 is quite efficient for the detoxification of MC-LR and MC-RR, and possesses significant bioremediation potential.

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Double-shell SnO@C hollow nanospheres were synthesized by a template method, and then the sulfur was loaded to form a cathode material of S/SnO@C composite. In Li-S batteries, it delivered a high initial specific capacity of 1473.1 mAh/g at a current density of 200 mA/g, and the capacity retention was even up to 95.7% over 100 cycles at 3200 mA/g, i.e., a capacity fade rate of only 0.043% per cycle. These good electrochemical performances should be attributed to the SnO@C hollow nanospheres. They can enhance the electronic conductivity by the outside carbon shell, and confine the lithium polysulfides by S-Sn-O and S-C chemical bonds to suppress the shuttle effect. Besides, the hollow nanospheres can readily accommodate the sulfur/sulfides to prevent the electrical/mechanical failure of the cathode, instead of their agglomeration on the external surface of SnO@C.

The degeneration of a regular heart rhythm into fibrillation (a chaotic or chaos-like sequence) can proceed via several classical routes described by nonlinear dynamics: period-doubling, quasiperiodicity, or intermittency. In this study, we experimentally examine one aspect of cardiac excitation dynamics, the long-term evolution of intracellular calcium signals in cultured cardiomyocyte networks subjected to increasingly faster pacing rates via field stimulation. In this spatially extended system, we observed alternans and higher-order periodicities, extra beats, and skipped beats or blocks. Calcium instabilities evolved nonmonotonically with the prevalence of phase-locking or Wenckebach rhythm, low-frequency magnitude modulations (signature of quasiperiodicity), and switches between patterns with occasional bursts (signature of intermittency), but period-doubling bifurcations were rare. Six ventricular-fibrillation-resembling episodes were pace-induced, for which significantly higher complexity was confirmed by approximate entropy calculations. The progressive destabilization of the heart rhythm by coexistent frequencies, seen in this study, can be related to theoretically predicted competition of control variables (voltage and calcium) at the single-cell level, or to competition of excitation and recovery at the cell network level. Optical maps of the response revealed multiple local spatiotemporal patterns, and the emergence of longer-period global rhythms as a result of wavebreak-induced reentries.

As titanium dioxide (TiO(2)) nanoparticles are widely used commercially, the potential effects of TiO(2) nanoparticles on humans are a concern. To evaluate the effects of TiO(2) nanoparticles on hepatic and renal functions and correlate changes to oxidative stress, Sprague-Dawley rats were treated with TiO(2) particles of two different specific surface areas (TiO(2-S50): 50 m(2)/g, and TiO(2-S210): 210 m(2)/g) at 0.5, 5, or 50 mg/kg body weight by intratracheal instillation. After 7 d, TiO(2) nanoparticles produced no obvious acute toxicity on hepatic and renal functions. However, superoxide dismutase (SOD) activity of plasma and glutathione peroxidase (GSH-PX) activity of kidney in the low-dose TiO(2-S210) group were significantly decreased. After TiO(2-S210) exposure, malondialdehyde (MDA) levels of liver and kidney in intermediate and high-dose groups were significantly increased. This change only appeared in liver after TiO(2-S50) exposure. Furthermore, SOD activity in liver and kidney and GSH-PX activity in kidney with low TiO(2-S210) exposure group were significantly less than with low TiO(2-S50). No apparent pathological changes in liver and kidney were observed. Intratracheal exposure to TiO(2) nanoparticles may induce oxidative stress in liver and kidney, but does not influence hepatic or renal functions. There was no apparent evidence that TiO(2-S210) was more toxic than TiO(2-S50). In general, intratracheal exposure to TiO(2) did not markedly affect extrapulmonary tissue functions.