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VPNET: Varying Screening machine Networks.
The pressing need to restart socioeconomic activities locked-down to control the spread of SARS-CoV-2 in Italy must be coupled with effective methodologies to selectively relax containment measures. Here we employ a spatially explicit model, properly attentive to the role of inapparent infections, capable of estimating the expected unfolding of the outbreak under continuous lockdown (baseline trajectory); assessing deviations from the baseline, should lockdown relaxations result in increased disease transmission; calculating the isolation effort required to prevent a resurgence of the outbreak. A 40% increase in effective transmission would yield a rebound of infections. A control effort capable of isolating daily ~5.5% of the exposed and highly infectious individuals proves necessary to maintain the epidemic curve onto the decreasing baseline trajectory. We finally provide an ex-post assessment based on the epidemiological data that became available after the initial analysis and estimate the actual disease transmission that occurred after weakening the lockdown.The structural organization of excitatory inputs supporting spike-timing-dependent plasticity (STDP) remains unknown. We performed a spine STDP protocol using two-photon (2P) glutamate uncaging (pre) paired with postsynaptic spikes (post) in layer 5 pyramidal neurons from juvenile mice. Here we report that pre-post pairings that trigger timing-dependent LTP (t-LTP) produce shrinkage of the activated spine neck and increase in synaptic strength; and post-pre pairings that trigger timing-dependent LTD (t-LTD) decrease synaptic strength without affecting spine shape. Furthermore, the induction of t-LTP with 2P glutamate uncaging in clustered spines (40 μm. These results indicate that synaptic cooperativity disrupts t-LTD and extends the temporal window for the induction of t-LTP, leading to STDP only encompassing LTP.Mangrove forests hold some of the highest densities of carbon recorded in any ecosystem, but have experienced widespread deforestation through conversion to aquaculture and agriculture. Alongside deforestation, mangroves have shown simultaneous natural expansion in some parts of the world, and considerable investments have been made into restoration programmes. Here we estimate net changes in the global mangrove carbon stock due to land cover change between 1996 and 2016, using data on mangrove deforestation and forestation, and proportional changes in carbon stock during processes of mangrove loss and gain. The global mangrove carbon stock declined by 158.4 Mt (95% CI = -156.8-525.9 Mt); a reduction of 1.8% of the stock present in 1996. Efforts to conserve and restore mangroves appear to have had some success, and - along with natural forestation - have contributed to relatively low net losses of mangrove carbon stocks over two decades.Nanoscale mineralized collagen fibrils may be important determinants of whole-bone mechanical properties and contribute to the risk of age-related fractures. read more In a cross-sectional study nano- and tissue-level mechanics were compared across trabecular sections from the proximal femora of three groups (n = 10 each) ageing non-fractured donors (Controls); untreated fracture patients (Fx-Untreated); bisphosphonate-treated fracture patients (Fx-BisTreated). Collagen fibril, mineral and tissue mechanics were measured using synchrotron X-Ray diffraction of bone sections under load. Mechanical data were compared across groups, and tissue-level data were regressed against nano. Compared to controls fracture patients exhibited significantly lower critical tissue strain, max strain and normalized strength, with lower peak fibril and mineral strain. Bisphosphonate-treated exhibited the lowest properties. In all three groups, peak mineral strain coincided with maximum tissue strength (i.e. ultimate stress), whilst peak fibril strain occurred afterwards (i.e. higher tissue strain). Tissue strain and strength were positively and strongly correlated with peak fibril and mineral strains. Age-related fractures were associated with lower peak fibril and mineral strain irrespective of treatment. Indicating earlier mineral disengagement and the subsequent onset of fibril sliding is one of the key mechanisms leading to fracture. Treatments for fragility should target collagen-mineral interactions to restore nano-scale strain to that of healthy bone.While footprinting analysis of ATAC-seq data can theoretically enable investigation of transcription factor (TF) binding, the lack of a computational tool able to conduct different levels of footprinting analysis has so-far hindered the widespread application of this method. Here we present TOBIAS, a comprehensive, accurate, and fast footprinting framework enabling genome-wide investigation of TF binding dynamics for hundreds of TFs simultaneously. We validate TOBIAS using paired ATAC-seq and ChIP-seq data, and find that TOBIAS outperforms existing methods for bias correction and footprinting. As a proof-of-concept, we illustrate how TOBIAS can unveil complex TF dynamics during zygotic genome activation in both humans and mice, and propose how zygotic Dux activates cascades of TFs, binds to repeat elements and induces expression of novel genetic elements.Epidemiological studies indicate that obesity negatively affects the progression and treatment of cervical-uterine cancer. Recent evidence shows that a subpopulation of adipose-derived stem cells can alter cancer properties. In the present project, we described for the first time the impact of adipose-derived stem cells over the malignant behavior of cervical cancer cells. The transcriptome of cancer cells cultured in the presence of stem cells was analyzed using RNA-seq. Changes in gene expression were validated using digital-PCR. Bioinformatics tools were used to identify the main transduction pathways disrupted in cancer cells due to the presence of stem cells. In vitro and in vivo assays were conducted to validate cellular and molecular processes altered in cervical cancer cells owing to stem cells. Our results show that the expression of 95 RNAs was altered in cancer cells as a result of adipose-derived stem cells. Experimental assays indicate that stem cells provoke an increment in migration, invasion, angiogenesis, and tumorigenesis of cancer cells; however, no alterations were found in proliferation.
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