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The multitude of forest die-off events within the last decade strongly suggests that forest mortality is an emerging global phenomenon, constituting a major uncertainty in projections of climate impacts on terrestrial ecosystems, climate-ecosystem interactions, and carbon-cycle feedbacks. This Review considers the societal and ecological consequences of dying forests. Forests provide innumerable ecological, societal and climatological benefits, yet they are vulnerable to drought and temperature extremes. Climate-driven forest die-off from drought and heat stress has occurred around the world, is expected to increase with climate change and probably has distinct consequences from those of other forest disturbances. We examine the consequences of drought- and climate-driven widespread forest loss on ecological communities, ecosystem functions, ecosystem services and land–climate interactions. Furthermore, we highlight research gaps that warrant study. As the global climate continues to warm, understanding the implications of forest loss triggered by these events will be of increasing importance.

Observations of the young star HD 142527, whose disk is separated into inner and outer regions by a gap suggestive of the formation of a gaseous giant planet, show that accretion onto the star is maintained by a flow of gas across the gap, in agreement with dynamical models of planet formation. Gas giants leave their mark According to current theories, giant planet formation carves a deep gap in the gas and dust around a protostar, clearing most of the dust and some of the gas away to form a ring-shaped cavity. But such a gap would rapidly turn off further growth in the mass of the star unless the abundant gas from the outer disk could traverse it. This paper presents Atacama Large Millimeter/submillimeter Array observations of the disk around the young star HD 142527 that reveal diffuse CO inside the gap and denser HCO + gas along gap-crossing filaments. The estimated gas flow across the gap would be sufficient to maintain accretion onto the star at the present rate. The formation of gaseous giant planets is thought to occur in the first few million years after stellar birth. Models 1 predict that the process produces a deep gap in the dust component (shallower in the gas 2 , 3 , 4 ). Infrared observations of the disk around the young star HD 142527 (at a distance of about 140 parsecs from Earth) found an inner disk about 10 astronomical units ( au ) in radius 5 (1  au is the Earth–Sun distance), surrounded by a particularly large gap 6 and a disrupted 7 outer disk beyond 140  au . This disruption is indicative of a perturbing planetary-mass body at about 90  au . Radio observations 8 , 9 indicate that the bulk mass is molecular and lies in the outer disk, whose continuum emission has a horseshoe morphology 8 . The high stellar accretion rate 10 would deplete the inner disk 11 in less than one year, and to sustain the observed accretion matter must therefore flow from the outer disk and cross the gap. In dynamical models, the putative protoplanets channel outer-disk material into gap-crossing bridges that feed stellar accretion through the inner disk 12 . Here we report observations of diffuse CO gas inside the gap, with denser HCO + gas along gap-crossing filaments. The estimated flow rate of the gas is in the range of 7 × 10 −9 to 2 × 10 −7 solar masses per year, which is sufficient to maintain accretion onto the star at the present rate.

Key Points Tumour resistance to chemotherapy and molecularly targeted therapies limits the effectiveness of current cancer therapies. Toxicity to normal tissues limits the amount of drug that can be systemically administered, and pharmacokinetic effects (absorption, distribution, metabolism and elimination (ADME)) limit the amount of drug that reaches the tumour. At the level of the tumour, various resistance mechanisms can operate, such as increased drug efflux, mutations of the drug target, DNA damage repair, activation of alternative signalling pathways and evasion of cell death. Tumour resistance can be intrinsic (that is, present before treatment), or acquired during treatment by various therapy-induced adaptive responses. Tumours are heterogeneous; therefore, resistance can also arise by positive selection of a drug-resistant tumour subpopulation. High-throughput screening techniques and systems biology approaches have the power to identify novel mechanisms of drug resistance and molecular signatures and genotypes that predict tumour response. Increasingly, predictive biomarkers will be used clinically to stratify patients to receive specific therapeutics. Improved understanding of the molecular basis of resistance will inevitably lead to the clinical assessment of rational drug combinations in selected patient populations. This Review discusses mechanisms of resistance to 'classical' cytotoxic chemotherapeutics and molecularly targeted therapies, which share many features. It is hoped that an improved understanding of the molecular basis of resistance will lead to rational drug combinations and predictive biomarkers. Resistance to chemotherapy and molecularly targeted therapies is a major problem facing current cancer research. The mechanisms of resistance to 'classical' cytotoxic chemotherapeutics and to therapies that are designed to be selective for specific molecular targets share many features, such as alterations in the drug target, activation of prosurvival pathways and ineffective induction of cell death. With the increasing arsenal of anticancer agents, improving preclinical models and the advent of powerful high-throughput screening techniques, there are now unprecedented opportunities to understand and overcome drug resistance through the clinical assessment of rational therapeutic drug combinations and the use of predictive biomarkers to enable patient stratification.

A case report is a narrative that describes, for medical, scientific, or educational purposes, a medical problem experienced by one or more patients. Case reports written without guidance from reporting standards are insufficiently rigorous to guide clinical practice or to inform clinical study design. Develop, disseminate, and implement systematic reporting guidelines for case reports. We used a three-phase consensus process consisting of (1) pre-meeting literature review and interviews to generate items for the reporting guidelines, (2) a face-to-face consensus meeting to draft the reporting guidelines, and (3) post-meeting feedback, review, and pilot testing, followed by finalization of the case report guidelines. This consensus process involved 27 participants and resulted in a 13-item checklist—a reporting guideline for case reports. The primary items of the checklist are title, key words, abstract, introduction, patient information, clinical findings, timeline, diagnostic assessment, therapeutic interventions, follow-up and outcomes, discussion, patient perspective, and informed consent. We believe the implementation of the CARE (CAse REport) guidelines by medical journals will improve the completeness and transparency of published case reports and that the systematic aggregation of information from case reports will inform clinical study design, provide early signals of effectiveness and harms, and improve healthcare delivery.