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Abstract Studies of microbial communities vary widely in terms of analysis methods. In this growing field, the wide variety of diversity measures and lack of consistency make it harder to compare different studies. Most existing alpha diversity metrics are inherited from other disciplines and their assumptions are not always directly meaningful or true for microbiome data. Many existing microbiome studies apply one or some alpha diversity metrics with no fundamentals but also an unclear results interpretation. This work focuses on a theoretical, empirical, and comparative analysis of 19 frequently and less-frequently used microbial alpha diversity metrics grouped into 4 proposed categories, including key features of every analyzed metric with their mathematical assumptions, to provide a deeper understanding of the existing metrics and a practical implementation guide for future studies. Key metrics that should be required in microbiome analysis include richness, phylogenetic diversity, entropy, dominance of a few microbes over others, and an estimate of unobserved microbes. Collectively, these metrics contribute to a comprehensive set of analyses characterizing samples, allowing the determination of key aspects that might be otherwise obscured by partial or biased information. These guidelines enable further detailed analysis by each author according to their specific interests and clinical trials. Several practical examples are provided to illustrate how these recommendations improve the quality and depth of information obtained, facilitating better interpretation when working with microbiome data. These guidelines can be applied to both existing and future research studies, enhancing the standardization, consistency, and robustness of the analyses conducted. This approach aims to improve the capture of biological diversity, leading to better interpretations and insights.

Motion is key to enzymatic catalysis. Gauto et al. show that a flexible loop region is crucial for the function of an aminopeptidase and show that magic-angle spinning NMR provides atomic-level quantitative insights in this very large complex.

El presente trabajo está centrado en mostrar las po sibilidades epistemológicas que la psicología tiene a su haber actualmente al enfrentarse a la in clusión de la noción de signo lingüístico, introducida por Lacan a través de su enseñanza, en la teoría y práctica del psicoanálisis. Específicamente esta ponencia está enfocada en most rar qué de relevante tiene la inclusión de esta noción, para nosotros como psicólogos y en nue stra práctica –teniendo en cuenta que el término nuestra práctica , comporta necesidades pedagógicas para la causa de esta ponencia, más que la proposición de un acuerdo entre nuestras pos iciones-. En este sentido, esta ponencia se guía por la línea temática de enfoque y epistemología de la psicología , aunque a mi parecer, debido a la importancia que el tema convoca, es tra nsversal a todas las líneas temáticas. Así mismo, intenta mostrar la transversalidad del texto lacaniano; el texto lacaniano como transversal a nuestra disciplina .

Mycobacterium tuberculosis, the causative agent of human tuberculosis, has two proteins belonging to the truncated hemoglobin (trHb) family. Mt-trHbN presents well-defined internal hydrophobic tunnels that allow O2 and •NO to migrate easily from the solvent to the active site, whereas Mt-trHbO possesses tunnels interrupted by a few bulky residues, particularly a tryptophan at position G8. Differential ligand migration rates allow Mt-trHbN to detoxify •NO, a crucial step for pathogen survival once under attack by the immune system, much more efficiently than Mt-trHbO. In order to investigate the differences between these proteins, we performed experimental kinetic measurements, •NO decomposition, as well as molecular dynamics simulations of the wild type Mt-trHbN and two mutants, VG8F and VG8W. These mutations affect both the tunnels accessibility as well as the affinity of distal site water molecules, thus modifying the ligand access to the iron. We found that a single mutation allows Mt-trHbN to acquire ligand migration rates comparable to those observed for Mt-trHbO, confirming that ligand migration is regulated by the internal tunnel architecture as well as by water molecules stabilized in the active site.

CO recombination kinetics has been investigated in the type II truncated hemoglobin from Thermobifida fusca (Tf-trHb) over more than 10 time decades (from 1 ps to ∼100 ms) by combining femtosecond transient absorption, nanosecond laser flash photolysis and optoacoustic spectroscopy. Photolysis is followed by a rapid geminate recombination with a time constant of ∼2 ns representing almost 60% of the overall reaction. An additional, small amplitude geminate recombination was identified at ∼100 ns. Finally, CO pressure dependent measurements brought out the presence of two transient species in the second order rebinding phase, with time constants ranging from ∼3 to ∼100 ms. The available experimental evidence suggests that the two transients are due to the presence of two conformations which do not interconvert within the time frame of the experiment. Computational studies revealed that the plasticity of protein structure is able to define a branched pathway connecting the ligand binding site and the solvent. This allowed to build a kinetic model capable of describing the complete time course of the CO rebinding kinetics to Tf-trHb.

Mycobacterium tuberculosis, the causative agent of human tuberculosis, has two proteins belonging to the truncated hemoglobin (trHb) family. Mt-trHbN presents well-defined internal hydrophobic tunnels that allow O 2 and •NO to migrate easily from the solvent to the active site, whereas Mt-trHbO possesses tunnels that are partially blocked by a few bulky residues, particularly a tryptophan at position G8. Differential ligand migration rates allow Mt-trHbN to detoxify •NO, a crucial step for pathogen survival once under attack by the immune system, much more efficiently than Mt-trHbO. In order to investigate the differences between these proteins, we performed experimental kinetic measurements, •NO decomposition, as well as molecular dynamics simulations of the wild type Mt-trHbN and two mutants, VG8F and VG8W. These mutations introduce modifications in both tunnel topologies and affect the incoming ligand capacity to displace retained water molecules at the active site. We found that a single mutation allows Mt-trHbN to acquire ligand migration rates comparable to those observed for Mt-trHbO, confirming that ligand migration is regulated by the internal tunnel architecture as well as by water molecules stabilized in the active site.