Notes

Programmed one-click getting yourself ready hippocampal-avoidance whole-brain irradiation inside RayStation.
Human speech production requires the ability to couple motor actions with their auditory consequences. Nonhuman primates might not have speech because they lack this ability. To address this question, we trained macaques to perform an auditory-motor task producing sound sequences via hand presses on a newly designed device ("monkey piano"). Catch trials were interspersed to ascertain the monkeys were listening to the sounds they produced. Functional MRI was then used to map brain activity while the animals listened attentively to the sound sequences they had learned to produce and to two control sequences, which were either completely unfamiliar or familiar through passive exposure only. All sounds activated auditory midbrain and cortex, but listening to the sequences that were learned by self-production additionally activated the putamen and the hand and arm regions of motor cortex. These results indicate that, in principle, monkeys are capable of forming internal models linking sound perception and production in motor regions of the brain, so this ability is not special to speech in humans. However, the coupling of sounds and actions in nonhuman primates (and the availability of an internal model supporting it) seems not to extend to the upper vocal tract, that is, the supralaryngeal articulators, which are key for the production of speech sounds in humans. The origin of speech may have required the evolution of a "command apparatus" similar to the control of the hand, which was crucial for the evolution of tool use.Whether real-world complex networks are scale free or not has long been controversial. Recently, in Broido and Clauset [A. D. Broido, A. Clauset, Nat. Commun. 10, 1017 (2019)], it was claimed that the degree distributions of real-world networks are rarely power law under statistical tests. Here, we attempt to address this issue by defining a fundamental property possessed by each link, the degree-degree distance, the distribution of which also shows signs of being power law by our empirical study. Surprisingly, although full-range statistical tests show that degree distributions are not often power law in real-world networks, we find that in more than half of the cases the degree-degree distance distributions can still be described by power laws. To explain these findings, we introduce a bidirectional preferential selection model where the link configuration is a randomly weighted, two-way selection process. The model does not always produce solid power-law distributions but predicts that the degree-degree distance distribution exhibits stronger power-law behavior than the degree distribution of a finite-size network, especially when the network is dense. We test the strength of our model and its predictive power by examining how real-world networks evolve into an overly dense stage and how the corresponding distributions change. We propose that being scale free is a property of a complex network that should be determined by its underlying mechanism (e.g., preferential attachment) rather than by apparent distribution statistics of finite size. We thus conclude that the degree-degree distance distribution better represents the scale-free property of a complex network.The gap junction protein Connexin 43 (Cx43) contributes to cell fate decisions that determine the location of fin ray joints during regeneration. Here, we provide insights into how Cx43, expressed medially, influences changes in gene expression in lateral skeletal precursor cells. Using the Gap27 peptide inhibitor specific to Cx43, we show that Cx43-gap junctional intercellular communication (GJIC) influences Cx43-dependent skeletal phenotypes, including segment length. We also demonstrate that Cx43-GJIC influences the expression of the Smp/β-catenin pathway in the lateral skeletal precursor cells, and does not influence the Sema3d pathway. Moreover, we show that the cx43lh10 allele, which has increased Cx43 protein levels, exhibits increased regenerate length and segment length. These phenotypes are rescued by Gap27, suggesting that increased Cx43 is responsible for the observed Cx43 phenotypes. Finally, our findings suggest that inhibition of Cx43 hemichannel activity does not influence Cx43-dependent skeletal phenotypes. These data provide evidence that Cx43-GJIC is responsible for regulating cell fate decisions associated with appropriate joint formation in the regenerating fin.The ways in which placental defects affect embryonic development are largely overlooked because of the lack of a trophoblast-specific approach for conditional gene ablation. To tackle this, we have established a simple, fast and efficient method for trophectodermal Tat-Cre/loxP recombination. We used the natural permeability barrier in mouse blastocysts in combination with off-the-shelf Tat-Cre recombinase to achieve editing of conditional alleles in the trophoblast lineage. This direct approach enables gene function analysis during implantation and placentation in mice, thereby crucially helping to broaden our understanding of human reproduction and development.Caenorhabditis elegans early embryos generate cell-specific transcriptomes despite lacking active transcription, thereby presenting an opportunity to study mechanisms of post-transcriptional regulatory control. We observed that some cell-specific mRNAs accumulate non-homogenously within cells, localizing to membranes, P granules (associated with progenitor germ cells in the P lineage) and P-bodies (associated with RNA processing). The subcellular distribution of transcripts differed in their dependence on 3'UTRs and RNA binding proteins, suggesting diverse regulatory mechanisms. Notably, we found strong but imperfect correlations between low translational status and P granule localization within the progenitor germ lineage. By uncoupling translation from mRNA localization, we untangled a long-standing question Are mRNAs directed to P granules to be translationally repressed, or do they accumulate there as a consequence of this repression? We found that translational repression preceded P granule localization and could occur independently of it. Further, disruption of translation was sufficient to send homogenously distributed mRNAs to P granules. https://www.selleckchem.com/products/nec-1s-7-cl-o-nec1.html These results implicate transcriptional repression as a means to deliver essential maternal transcripts to the progenitor germ lineage for later translation.
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