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Insects are the most speciose group of animals, but the phylogenetic relationships of many major lineages remain unresolved. We inferred the phylogeny of insects from 1478 protein-coding genes. Phylogenomic analyses of nucleotide and amino acid sequences, with site-specific nucleotide or domain-specific amino acid substitution models, produced statistically robust and congruent results resolving previously controversial phylogenetic relationships. We dated the origin of insects to the Early Ordovician [~479 million years ago (Ma)], of insect flight to the Early Devonian (~406 Ma), of major extant lineages to the Mississippian (~345 Ma), and the major diversification of holometabolous insects to the Early Cretaceous. Our phylogenomic study provides a comprehensive reliable scaffold for future comparative analyses of evolutionary innovations among insects.

Due to massive energetic investments in woody support structures, trees are subject to unique physiological, mechanical, and ecological pressures not experienced by herbaceous plants. Despite a wealth of studies exploring trait relationships across the entire plant kingdom, the dominant traits underpinning these unique aspects of tree form and function remain unclear. Here, by considering 18 functional traits, encompassing leaf, seed, bark, wood, crown, and root characteristics, we quantify the multidimensional relationships in tree trait expression. We find that nearly half of trait variation is captured by two axes: one reflecting leaf economics, the other reflecting tree size and competition for light. Yet these orthogonal axes reveal strong environmental convergence, exhibiting correlated responses to temperature, moisture, and elevation. By subsequently exploring multidimensional trait relationships, we show that the full dimensionality of trait space is captured by eight distinct clusters, each reflecting a unique aspect of tree form and function. Collectively, this work identifies a core set of traits needed to quantify global patterns in functional biodiversity, and it contributes to our fundamental understanding of the functioning of forests worldwide.

Magnetoresistance is a change in the resistance of a material system caused by an applied magnetic field. Giant magnetoresistance occurs in structures containing ferromagnetic contacts separated by a metallic non-magnetic spacer, and is now the basis of read heads for hard drives and for new forms of random access memory. Using an insulator (for example, a molecular thin film) rather than a metal as the spacer gives rise to tunnelling magnetoresistance, which typically produces a larger change in resistance for a given magnetic field strength, but also yields higher resistances, which are a disadvantage for real device operation. Here, we demonstrate giant magnetoresistance across a single, non-magnetic hydrogen phthalocyanine molecule contacted by the ferromagnetic tip of a scanning tunnelling microscope. We measure the magnetoresistance to be 60% and the conductance to be 0.26 G 0 , where G 0 is the quantum of conductance. Theoretical analysis identifies spin-dependent hybridization of molecular and electrode orbitals as the cause of the large magnetoresistance. A single magnetic molecule between ferromagnetic contacts exhibits a 60% magnetoresistance effect and nearly metallic conduction at the same time.

For decades, scientists have been raising calls for societal changes that will reduce our impacts on nature. Though much conservation has occurred, our natural environment continues to decline under the weight of our consumption. Humanity depends directly on the output of nature; thus, this decline will affect us, just as it does the other species with which we share this world. Díaz et al. review the findings of the largest assessment of the state of nature conducted as of yet. They report that the state of nature, and the state of the equitable distribution of nature's support, is in serious decline. Only immediate transformation of global business-as-usual economies and operations will sustain nature as we know it, and us, into the future. Science , this issue p. eaax3100 The human impact on life on Earth has increased sharply since the 1970s, driven by the demands of a growing population with rising average per capita income. Nature is currently supplying more materials than ever before, but this has come at the high cost of unprecedented global declines in the extent and integrity of ecosystems, distinctness of local ecological communities, abundance and number of wild species, and the number of local domesticated varieties. Such changes reduce vital benefits that people receive from nature and threaten the quality of life of future generations. Both the benefits of an expanding economy and the costs of reducing nature’s benefits are unequally distributed. The fabric of life on which we all depend—nature and its contributions to people—is unravelling rapidly. Despite the severity of the threats and lack of enough progress in tackling them to date, opportunities exist to change future trajectories through transformative action. Such action must begin immediately, however, and address the root economic, social, and technological causes of nature’s deterioration.

Despite many years of research, no biomarkers for stroke are available to use in clinical practice. Progress in high-throughput technologies has provided new opportunities to understand the pathophysiology of this complex disease, and these studies have generated large amounts of data and information at different molecular levels. The integration of these multi-omics data means that thousands of proteins (proteomics), genes (genomics), RNAs (transcriptomics) and metabolites (metabolomics) can be studied simultaneously, revealing interaction networks between the molecular levels. Integrated analysis of multi-omics data will provide useful insight into stroke pathogenesis, identification of therapeutic targets and biomarker discovery. In this Review, we detail current knowledge on the pathology of stroke and the current status of biomarker research in stroke. We summarize how proteomics, metabolomics, transcriptomics and genomics are all contributing to the identification of new candidate biomarkers that could be developed and used in clinical stroke management.In this Review, Montaner and colleagues summarize how proteomics, genomics, transcriptomics and metabolomics are contributing to the discovery and development of biomarkers in stroke, and how bringing them together with integromics could provide new biomarkers and therapeutic opportunities.

Improving equity is an emerging priority in climate and energy strategies, but little is known how these strategies would alter inequalities. Regional inequalities such as price, employment and land use are especially relevant in the electricity sector, which must decarbonize first to allow other sectors to decarbonize. Here, we show that a European low-carbon electricity sector in 2035 can reduce but also sustain associated regional inequalities. Using spatially-explicit modeling for 296 sub-national regions, we demonstrate that emission cuts consistent with net-zero greenhouse gas emissions in 2050 result in continent-wide benefits by 2035 regarding electricity sector investments, employment gains, and decreased greenhouse gas and particulate matter emissions. However, the benefits risk being concentrated in affluent regions of Northern Europe, while regions of Southern and Southeastern Europe risk high vulnerabilities due to high adverse impacts and sensitivities, and low adaptive capacities. Future analysis should investigate policy mechanisms for reducing and compensating inequalities. The low-carbon electricity sector in Europe can bring overall benefits of new investment, employment, and decreased emissions, but could sustain regional inequalities between Northern and Southern Europe.

High-grade serous ovarian carcinoma (HGSOC) is the most frequent type of ovarian cancer and has a poor outcome. It has been proposed that fallopian tube cancers may be precursors of HGSOC but evolutionary evidence for this hypothesis has been limited. Here, we perform whole-exome sequence and copy number analyses of laser capture microdissected fallopian tube lesions (p53 signatures, serous tubal intraepithelial carcinomas (STICs), and fallopian tube carcinomas), ovarian cancers, and metastases from nine patients. The majority of tumor-specific alterations in ovarian cancers were present in STICs, including those affecting TP53, BRCA1 , BRCA2 or PTEN . Evolutionary analyses reveal that p53 signatures and STICs are precursors of ovarian carcinoma and identify a window of 7 years between development of a STIC and initiation of ovarian carcinoma, with metastases following rapidly thereafter. Our results provide insights into the etiology of ovarian cancer and have implications for prevention, early detection and therapeutic intervention of this disease. It has previously been proposed that high-grade serous ovarian carcinoma (HGSOC) may originate from the fallopian tube. Here, the authors analyze genetic aberrances in fallopian tube lesions, ovarian cancers, and metastases from HGSOC patients and establish the evolutionary origins of HGSOC in the fallopian tube.

Many eukaryotic cells grow by extending their cell periphery in pulses. The molecular mechanisms underlying this process are not yet fully understood. Here we present a comprehensive model of stepwise cell extension by using the unique tip growth system of filamentous fungi. Live-cell imaging analysis, including superresolution microscopy, revealed that the fungus Aspergillus nidulans extends the hyphal tip in an oscillatory manner. The amount of F-actin and secretory vesicles (SV) accumulating at the hyphal tip oscillated with a positive temporal correlation, whereas vesicle amounts were negatively correlated to the growth rate. The intracellular Ca2+ level also pulsed with a positive temporal correlation to the amount of F-actin and SV at the hyphal tip. Two Ca2+ channels, MidA and CchA, were needed for proper tip growth and the oscillations of actin polymerization, exocytosis, and the growth rate. The data indicate a model in which transient Ca2+ pluses cause depolymerization of F-actin at the cortex and promote SV fusion with the plasma membrane, thereby extending the cell tip. Over time, Ca2+ diffuses away and F-actin and SV accumulate again at the hyphal tip. Our data provide evidence that temporally controlled actin polymerization and exocytosis are coordinated by pulsed Ca2+ influx, resulting in stepwise cell extension.

The present procedural guidelines summarize the current views of the EANM Neuro-Imaging Committee (NIC). The purpose of these guidelines is to assist nuclear medicine practitioners in making recommendations, performing, interpreting, and reporting results of [ 18 F]FDG-PET imaging of the brain. The aim is to help achieve a high-quality standard of [ 18 F]FDG brain imaging and to further increase the diagnostic impact of this technique in neurological, neurosurgical, and psychiatric practice. The present document replaces a former version of the guidelines that have been published in 2009. These new guidelines include an update in the light of advances in PET technology such as the introduction of digital PET and hybrid PET/MR systems, advances in individual PET semiquantitative analysis, and current broadening clinical indications (e.g., for encephalitis and brain lymphoma). Further insight has also become available about hyperglycemia effects in patients who undergo brain [ 18 F]FDG-PET. Accordingly, the patient preparation procedure has been updated. Finally, most typical brain patterns of metabolic changes are summarized for neurodegenerative diseases. The present guidelines are specifically intended to present information related to the European practice. The information provided should be taken in the context of local conditions and regulations.

PurposeThis joint practice guideline or procedure standard was developed collaboratively by the European Association of Nuclear Medicine (EANM) and the Society of Nuclear Medicine and Molecular Imaging (SNMMI). The goal of this guideline is to assist nuclear medicine practitioners in recommending, performing, interpreting, and reporting the results of dopaminergic imaging in parkinsonian syndromes.MethodsCurrently nuclear medicine investigations can assess both presynaptic and postsynaptic function of dopaminergic synapses. To date both EANM and SNMMI have published procedural guidelines for dopamine transporter imaging with single photon emission computed tomography (SPECT) (in 2009 and 2011, respectively). An EANM guideline for D2 SPECT imaging is also available (2009). Since the publication of these previous guidelines, new lines of evidence have been made available on semiquantification, harmonization, comparison with normal datasets, and longitudinal analyses of dopamine transporter imaging with SPECT. Similarly, details on acquisition protocols and simplified quantification methods are now available for dopamine transporter imaging with PET, including recently developed fluorinated tracers. Finally, [18F]fluorodopa PET is now used in some centers for the differential diagnosis of parkinsonism, although procedural guidelines aiming to define standard procedures for [18F]fluorodopa imaging in this setting are still lacking.ConclusionAll these emerging issues are addressed in the present procedural guidelines for dopaminergic imaging in parkinsonian syndromes.