Genetic studies of human evolution require high-quality contiguous ape genome assemblies that are not guided by the human reference. We coupled long-read sequence assembly, full-length cDNA sequencing with a multi-platform scaffolding approach to produce ab initio chimpanzee and orangutan genome assemblies. Comparing these with two long-read de novo human genome assemblies and a gorilla genome assembly, we characterized lineage-specific and shared great ape genetic variation ranging from single base-pair to megabase-sized variants. We identified ~17 thousand fixed human-specific structural variants identifying genic and putative regulatory changes that emerged in humans since divergence from nonhuman apes. Interestingly, these fixed human-specific structural variants are enriched near genes that are downregulated in human compared to chimpanzee cerebral organoids, particularly in cells analogous to radial glial neural progenitors.

Gut microbes programme their metabolism to suit intestinal conditions and convert dietary components into a panel of small molecules that ultimately affect host physiology. To unveil what is behind the effects of key dietary components on microbial functions and the way they modulate host-microbe interaction, we used for the first time a multi-omic approach that goes behind the mere gut phylogenetic composition and provides an overall picture of the functional repertoire in 27 fecal samples from omnivorous, vegan and vegetarian volunteers. Based on our data, vegan and vegetarian diets were associated to the highest abundance of microbial genes/proteins responsible for cell motility, carbohydrate-and protein-hydrolyzing enzymes, transport systems and the synthesis of essential amino acids and vitamins. A positive correlation was observed when intake of fiber and the relative fecal abundance of flagellin were compared. Microbial cells and flagellin extracted from fecal samples of 61 healthy donors modulated the viability of the human (HT29) colon carcinoma cells and the host response through the stimulation of the expression of Toll-like receptor 5, lectin RegIIIα and three interleukins (IL-8, IL-22 and IL-23). Our findings concretize a further and relevant milestone on how the diet may prevent/mitigate disease risk. Comprising 10 12-14 cells from 100-1000 species, the human intestinal microbiome is a complex entity living in our body. It affects human health, sustenance and well-being 1. Functioning as an extra organ 2 , the intestinal microbiome uses nutrients from ingested foods, releases harmful or beneficial metabolites and regulates the immune system 3,4. Dysbiosis of the intestinal microbiome has been associated to various gastrointestinal (GI) and non-GI diseases, such as obesity, heart-, kidney-and liver-related diseases, cancer and autism 5-7 , but the dilemma whether it acts as cause or consequence remains too far from the solution. Because the simple phylogenetic characterization does not provide deep information on functional repertoires 8,9 , a number of projects and studies have employed the whole-community shotgun sequencing to combine the composition and gene content of the human intestinal microbiome 2,10. Current meta-genomic data show limited differences among individuals, which hypothesize the existence of a stable core microbiome and similar metabolic traits 10. Notwithstanding the relevance of these findings, they do not necessarily imply similar in vivo microbial activities. Indeed, a panel of factors (e.g., diet, host genetics and pharmacological treatments) markedly affect such activities 11. Dietary components have the capability to modulate the composition and mainly the function of the intestinal microbiome 3,12,13. Correlations between entero-gradients/types and vegetable-rich (Prevotella and Lachnospira) or animal protein-rich diets (Bacteroides and Clostridia/Ruminococcus) have been already highlighted 12,14 , but the impact of dietary components still remains unclear. Previously, we...

Critical micelle concentration (CMC) is the main chemical–physical parameter to be determined for pure surfactants for their characterization in terms of surface activity and self-assembled aggregation. The CMC values can be calculated from different techniques ( e.g ., tensiometry, conductivity, fluorescence spectroscopy), able to follow the variation of a physical property with surfactant concentrations. Different mathematical approaches have been applied for the determination of CMC values from the raw experimental data. Most of them are independent of the operator, despite not all of the fitting procedures employed so far can be applied in all techniques. In this experimental work, the second derivative of the experimental data has been proposed as a unique approach to determine the CMC values from different techniques (tensiometry, conductimetry, densimetry, spectrofluorimetry, and high-resolution ultrasound spectroscopy). To this end, the CMC values of five different surfactants, specifically three anionic (sodium dodecyl sulfate, sodium deoxycolate, and N -lauroyl sarcosinate) and two nonionic, such as polyethylene glycol ester surfactants [polyethylenglicol (8) monostearate and polyethylenglicol (8) monolaurate], have been determined by this approach. The “second-derivate” approach provides a reliable determination of the CMC values among all of the techniques investigated, which were comparable to those calculated by the other operator-free routinely methods employed, such as segmental linear regression or Boltzmann regression. This study also highlighted the strengths and shortcomings of each technique over the others, providing an overview of the CMC values of commonly used anionic and nonionic surfactants in the pharmaceutical field, determined by employing different experimental approaches.

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During June 2022, Spain was one of the countries most affected worldwide by a multicountry monkeypox outbreak with chains of transmission without identified links to disease-endemic countries. We provide epidemiologic features of cases reported in Spain and the coordinated measures taken to respond to this outbreak.