Notes

Evaluation of Tooth Program regarding Seniors Residing in Long-Term Care Facilities.
1 kb ROM and 3 kb program flash, consuming an average power of 130 μW.

The method presented has the advantages over other approaches, that it allows spike events to be robustly detected in real-time from neural activity in a completely autonomous way, without the need for any calibration, and can be implemented with low hardware resources.

The proposed method can detect spikes effectively and adaptively. It alleviates the need for re-calibration, which is critical towards achieving a viable BMI, and more so with future 'high bandwidth' systems' targeting 1000s of channels.
The proposed method can detect spikes effectively and adaptively. It alleviates the need for re-calibration, which is critical towards achieving a viable BMI, and more so with future 'high bandwidth' systems' targeting 1000s of channels.
Electroencephalogram (EEG) signals may be contaminated with muscle artifacts that are usually difficult to be removed.

In this article, a new hybrid method for suppressing muscle artifacts is proposed. Our method leverages variational mode decomposition (VMD) and canonical correlation analysis (CCA) algorithms. Each channel of EEG is decomposed into intrinsic mode functions (IMFs) with VMD to achieve an extended data set that contains more channels than the original data set. The potential artifact components are decomposed by CCA for further isolation.

The proposed method is evaluated with semi-simulation and real contaminated EEG signals. The results show that the performance of removing artifacts for VMD-CCA exceeds the comparison methods.

Regardless of the number of EEG channels and the signal-to-noise ratio of the signal, the VMD-CCA approach is superior to the existing methods. As the number of EEG channels decreases, the average de-artifact effects of VMD-CCA and the comparison approaches are basically the same, but the randomness increases.

The VMD-CCA method can effectively isolate muscle artifacts in EEG in case of multiple channels or few channels.
The VMD-CCA method can effectively isolate muscle artifacts in EEG in case of multiple channels or few channels.Cadmium (Cd) is a ubiquitous environmental and occupational pollutant that is considered as a high-risk factor for neurodegenerative diseases. However, the mechanism underlying Cd-induced neurotoxicity has not been fully elucidated. Abnormal mitochondrial distribution and excessive mitochondrial fission are increasingly implicated in various neurological pathologies. Herein, by exposing primary cortical neurons to Cd (10 and 100 μM) for various times (0, 6, 12, and 24 h), we observed that the rapid motility of the mitochondria in neurons progressively slowed. Many more mitochondria were transported and distributed to the somas of Cd-treated neurons. Coupled with abnormal mitochondrial distribution, Cd exposure triggered excessive mitochondrial fragmentation, followed by mitochondrial membrane potential loss and neuronal damage. Crenolanib mw However, BAPTA-AM, a chelator of cytosolic calcium ([Ca2+]c), significantly attenuated Cd-induced abnormal mitochondrial distribution and excessive mitochondrial fission, which protected against Cd-induced mitochondrial damage and neuronal toxicity. In contrast to the increase in [Ca2+]c, Cd exposure had no effect on the level of mitochondrial calcium ([Ca2+]m). Inhibiting [Ca2+]m uptake, either by ruthenium 360 (Ru360) or by knock-out of mitochondrial calcium uniporter (MCU), failed to alleviate Cd-induced mitochondrial damage and neuronal toxicity. Additionally, in MCU knock-out neurons, BAPTA-AM effectively prevented Cd-induced abnormal mitochondrial distribution and excessive mitochondrial fission. Taken together, Cd exposure disrupts mitochondrial distribution and activates excessive mitochondrial fission by elevating [Ca2+]c independent of MCU-mediated mitochondrial calcium uptake, thereby leading to neurotoxicity. Chelating overloaded [Ca2+]c is a promising strategy to prevent the neurotoxicity of Cd.Organophosphorus compounds (OP) causes prominent delayed neuropathy in vivo and cytotoxicity to neuronal cells in vitro. The primary target protein of OP's neurotoxicity is neuropathy target esterase (NTE), which can convert phosphatidylcholine (PC) to glycerophosphocholine (GPC). Recent studies reveal that autophagic cell death is important for the initiation and progression of OP-induced neurotoxicity both in vivo and in vitro. However, the mechanism of how OP induces autophagic cell death is unknown. Here it is found that GPC is an important organic osmolyte in the neuroblastoma cells, and treatment with tri-o-cresyl phosphate (TOCP), a representative OP, leads to the decrease of GPC and imbalance of extracellular and intracellular osmolality. Knockdown of GPC metabolizing enzyme glycerophosphodiester phosphodiesterase domain containing 5 (GDPD5) reverses TOCP-induced autophagic cell death, which further supports the notion that the reduced GPC level leads to the autophagic cell death. Furthermore, it is found that autophagic cell death is due to the induction of reactive oxygen species (ROS) and mitochondrial damage by imbalance of osmolality with TOCP treatment. In summary, this study reveals that TOCP treatment decreases GPC level and intracellular osmolality, which induces ROS and mitochondrial damage and leads to the cell death and neurite degradation by autophagy. This study lays the foundation for further investigations on the potential therapeutic approaches for OP neurotoxicity or NTE mutation-related neurological diseases.
A simultaneous integrated boost (SIB) leads to less acute toxicity. Less is known for late toxicity due to SIB. In this first and only randomized trial, two-years toxicity is analysed.

Physician-assessed toxicity, using the LENT SOMA scale, and photographs, analysed with the BCCT.core software, was examined for 150 patients, randomized between SIB and sequential boost (SEB).

Differences in physician-assessed two-years toxicity and photographic analysis between SIB and SEB are very small and not significant.

There is no indication that a SIB leads to an excess in toxicity or worse cosmetic outcome at 2years.
There is no indication that a SIB leads to an excess in toxicity or worse cosmetic outcome at 2 years.
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