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Some cytotoxic anticancer drugs may boost an immunogenic molecular signal of apoptosis.

A protein produced by parasitic roundworms that inhibits the inflammatory response is shown to prevent mast cell activation. The protein could potentially be used for the management of allergies and asthma (pages 1375–1381).

Two cell-based resources producing a broad repertoire of glycosaminoglycan structures will facilitate new applications in the glycosciences field and beyond.

New fabric-like sensors measure and transmit mechanical strain on the skin with unprecedented sensitivity.

Current attempts to block angiogenesis during cancer and other diseases are limited partly by their effects on normal angiogenic processes. Could a more targeted approach emerge from the identification of a factor required for pathological angiogenesis under conditions of hypoxia (pages 553–558)?

Here, the authors use simulated quantitative gut microbial communities to benchmark the performance of 13 common data transformations in determining diversity as well as microbe-microbe and microbe-metadata associations, finding that quantitative approaches incorporating microbial load variation outperform computational strategies in downstream analyses, urging for a widespread adoption of quantitative approaches, or recommending specific computational transformations whenever determination of microbial load of samples is not feasible.

Pfs48/45, a surface protein of Plasmodium falciparum, is a promising anti-malarial vaccine candidate whose structure is not entirely resolved. Here, the authors present the structure of the full-length molecule, and characterise the binding and activity of transmission blocking antibodies.

Growth factors used to accelerate engraftment after hematopoietic cell transplantation can increase the severity of graft-versus-host disease. Experiments with mice examine how irradiation, used to prepare recipients for transplants, contributes to this problem (pages 436–441).

Smad7 controls inflammation by negatively regulating activation of the transcription factor NF-κB. New work shows that Smad7 inhibits NF-κB by binding to the regulatory proteins TAB2 and TAB3, thereby blocking association of the E3 ubiquitin ligase TRAF2 with the kinase TAK1.

An exciting genome-wide association study in the British population for seven common diseases. This analysis confirms previously identified loci and provides strong evidence for many novel disease susceptibility loci.

Promoting angiogenesis—rather than blocking it—may represent a new strategy for killing tumors.

The United Nations Sustainable Development Goals outline a roadmap towards a more equitable future for humanity. Along with other scientists, physicists have long made valuable contributions to this endeavour.

Optogenetic tools enable precise experimental control of the behaviour of cells. Here, the authors introduce a genetically-encoded two-protein system that enables silencing of excitable cells such as neurons and cardiomyocytes using blue light, and demonstrate its utility both in vitro and In vivo.

Despite having an increasingly accurate parts list for biological cells, much is left to discover about how these parts act together to create functional cells, and how distinct individual cells interact to create functional tissues and organs. Biologists are increasingly aware of the cell-to-cell variability in molecule copy numbers—a trend that is revealed by several new techniques, including one that permits counting molecules in single cells.

Wnt signaling has been shown to be involved in stem cell regulation and may represent a key pathway in controlling hematopoiesis. But is it possible for hematopoietic stem cells to get too much of a good thing?

The role of inflammatory mechanisms in amyotrophic lateral sclerosis is a hotly debated topic. Findings in a mouse model now add weight to arguments that targeting of inflammatory cells might be a fruitful therapeutic approach.

Precision-spectroscopy techniques can accurately measure lines in constrained frequency and intensity ranges. The authors propose a spectroscopic-network-assisted precision spectroscopy method by which transitions measured in a narrow range provide information in other, extended regions of the spectrum.

Alzheimer’s disease is characterized by the aggregation of the Abeta peptide and the tau protein. Here the authors track the formation of wild-type or mutant tau oligomers through to large aggregates and gain insights into the molecular basis of how tau mutations cause disease by altering the aggregation pathway.

Sepsis is by no means a single clinical entity; physicians must battle a variety of syndromes with only a vague notion of the molecular events that connect them. This vagueness now begins to dissipate with the identification of a molecule that can prevent the development of acute septic shock and severe sepsis (pages 161–167).

A new article by Pandarinath et al. describes an artificial neural network model that captures some key aspects of the activity of populations of neurons in the primary motor cortex.

The mechanism allowing sperm to steer is not fully understood. The authors find that superposition of two harmonic waves breaks the flagellar beat symmetry temporally rather than spatially, and that this mechanism is enhanced by the sexual hormone progesterone, which changes the motility pattern.

A strain of Escherichia coli that causes urinary tract infections seems to take hold in the body by interfering with signaling through Toll-like receptors (TLRs). The mechanism involves a secreted bacterial protein that is taken up by cells and clogs up the TLR signaling mechanism (pages 399–406).

Wnt signals are seemingly ubiquitous in biology, controlling processes as diverse as bristle patterning in flies and tissue regeneration in humans. A new report describes the discovery of small molecules that inhibit Wnt signaling by two unprecedented mechanisms, paving the way for fundamental studies and perhaps improved treatment of colon cancer.

Different subsets of bone marrow stem cells can be mobilized by varying drug treatments.

The phosphatase SHIP2 has been the focus of drug development efforts for diabetes. This distinction is based in part on work suggesting that the molecule is central to the regulation of glucose levels in tissues and blood. An analysis of a SHIP2 knockout mouse changes this viewpoint and provides new directions for therapeutic intervention (pages 199–205).

Toll-like receptor signaling induces the production of proinflammatory cytokines and type I interferons. Inhibition of the kinase IRAK1 by the phosphatase SHP-1 provides reciprocal regulation of these pathways by dampening the former while enhancing the latter.

Thalidomide, a drug reviled in the 1960s for its teratogenic effects, has been revived in recent years for cancer and leprosy therapy. A study now finds another use for this drug in vascular disease, providing further insights into the drug's mechanisms of action (pages 420–428).

A new study identifies pikachurin, a previously-unknown dystroglycan-binding protein that is critical for the apposition of photoreceptor and bipolar cell dendrites at the ribbon synapse. This work could explain some of the visual defects seen in several muscular dystrophies.

Two studies suggest how mutations in the APC tumor suppressor gene can contribute to chromosomal aberrations in precancerous cells.

The identification of a functionally distinct thymus-dependent lineage of mouse natural killer cells demonstrates the diversity of the natural killer cell population.

Toll-like receptor (TLR) signaling must be tightly regulated to avoid uncontrolled inflammation. A fifth Toll–interleukin 1 receptor adaptor domain, SARM, has been identified as an inhibitor of TLR3 and TLR4 signaling.

A new and unexpected role is identified for Srebps in controlling NK cell activity that is independent of their role in lipid biosynthesis.

Copy number variants (CNVs) account for a major proportion of human genetic diversity and may contribute to genetic susceptibility to disease. Here, a large, genome-wide study of association between common CNVs and eight common human diseases is presented. The study provides a wealth of technical insights that will inform future study design and analysis. The results also indicate that common CNVs that can be 'typed' on existing platforms are unlikely to contribute much to the genetic basis of common diseases.

Smoke is a solid. Whether from cigarettes, cooking fires or other sources, it is comprised of tiny particles that injure the lung and can lead to lung cancer and chronic obstructive pulmonary disorder, characterized by laborious breathing. Steven D. Shapiro and his colleagues take a look at imaging data in people suggesting that these two conditions have more in common mechanistically than was previously thought. Both diseases seem to stem in part from the ability of inhaled particles to trigger inflammation, a process examined by Robert M. Senior and his colleagues.

Expression of a microRNA may underlie cardiac arrhythmias (pages 486–491).

Mycobacterium leprae, the bacterium that causes leprosy, causes the breakdown of myelin. This breakdown is now shown to occur through the ErbB2 receptor, a process that can be blocked by Herceptin and kinase inhibitors (pages 961–966).

A study finds that pain hypersensitivity in male and female mice is differentially dependent on microglia and T cells, and describes a sex-specific response to microglia-targeted pain treatments. This sex difference will be important to consider when developing treatments for pain and other neurological disorders involving microglia and immune cells.

A powerful technology called global protein stability profiling allows rates of protein turnover to be determined for a substantial fraction of the human proteome in a single experiment. This approach sets the stage for systems-level analyses of the dynamics of the mammalian proteome.

The streptococcal toxic shock syndrome causes a massive leak of plasma from the circulation, leading to low blood pressure and respiratory failure. Now this leakage is traced to the effects of neutrophils activated by a bacterial surface protein.

Fat cells secrete the hormone adiponectin, which regulates glucose metabolism through actions on peripheral tissues. It is now apparent that adiponectin also acts on the brain to reduce body weight and improve glucose metabolism (pages 524–529).

The capacity of Amazonian forests to sequester carbon has weakened with potentially important implications for climate change.

Recent papers shed insight into the architecture and dynamics of the components of the bacterial replisome.

The in situ cryo-electron microscopy structure of the intact Salmonella flagellar basal body—including the inner membrane rotor, drive shaft and outer membrane bushing complex—elucidates the mechanisms of assembly of this complex macromolecular structure that enables bacterial motility.