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Seafloor kitty over the Italian language resort sector: A method of identify reasons for marine kitten.
To inform its clinical utility, our strategy was adopted to track the temporal profile of circulating acetaminophen (a widely used analgesic and antipyretic) in saliva and sweat, using a surface-modified boron-doped diamond sensing interface (cross-validated with laboratory-based assays, R2 ∼ 0.94). Through integration of the engineered sensing interface within a custom-developed smartwatch, and augmentation with a dedicated analytical framework (for redox peak extraction), we realized a wearable solution to seamlessly render drug readouts with minute-level temporal resolution. Leveraging this solution, we demonstrated the pharmacokinetic correlation and significance of sweat readings.Changes in the way health insurers pay healthcare providers may not only directly affect the insurer's patients but may also affect patients covered by other insurers. We provide evidence of such spillovers in the context of a nationwide Medicare bundled payment reform that was implemented in some areas of the country but not in others, via random assignment. We estimate that the payment reform-which targeted traditional Medicare patients-had effects of similar magnitude on the healthcare experience of nontargeted, privately insured Medicare Advantage patients. We discuss the implications of these findings for estimates of the impact of healthcare payment reforms and more generally for the design of healthcare policy.The memory of our brain, stored in soft matter, is dynamic, and it forgets spontaneously to filter unimportant information. By contrast, the existing manmade memory, made from hard materials, is static, and it does not forget without external stimuli. Here we propose a principle for developing dynamic memory from soft hydrogels with temperature-sensitive dynamic bonds. The memorizing-forgetting behavior is achieved based on fast water uptake and slow water release upon thermal stimulus, as well as thermal-history-dependent transparency change of these gels. The forgetting time is proportional to the thermal learning time, in analogy to the behavior of brain. The memory is stable against temperature fluctuation and large stretching; moreover, the forgetting process is programmable. This principle may inspire future research on dynamic memory based on the nonequilibrium process of soft matter.People may be sympathetic to violent extremism when it serves their own interests. Such support may manifest itself via biased recognition of hate crimes. Psychological surveys were conducted in the wakes of mass shootings in the United States, New Zealand, and the Netherlands (total n = 2,332), to test whether factors that typically predict endorsement of violent extremism also predict biased hate crime perceptions. Path analyses indicated a consistent pattern of motivated judgment hate crime perceptions were directly biased by prejudicial attitudes and indirectly biased by an aggrieved sense of disempowerment and White/Christian nationalism. After the shooting at a synagogue in Pittsburgh, Pennsylvania, disempowerment-fueled anti-Semitism predicted lower perceptions that the gunman was motivated by hatred and prejudice (study 1). After the shootings that occurred at two mosques in Christchurch, New Zealand, disempowerment-fueled Islamoprejudice similarly predicted lower hate crime perceptions (study 2a). Conversely, after the tram shooting in Utrecht, Netherlands (which was perpetrated by a Turkish-born immigrant), disempowerment-fueled Islamoprejudice predicted higher hate crime perceptions (study 2b). Finally, after the Walmart shooting in El Paso, Texas, hate crime perceptions were specifically biased by an ethnonationalist view of Hispanic immigrants as a symbolic (rather than realistic) threat to America; that is, disempowered individuals deemphasized likely hate crimes due to symbolic concerns about cultural supremacy rather than material concerns about jobs or crime (study 3). BAY-985 nmr Altogether, biased hate crime perceptions can be purposive and reveal supremacist sympathies.Amino acids are naturally occurring and structurally diverse metabolites in biological system, whose potentials for chemical expansion, however, have not been fully explored. Here, we devise a metabolic platform capable of producing industrially important C3-C5 diols from amino acids. The presented platform combines the natural catabolism of charged amino acids with a catalytically efficient and thermodynamically favorable diol formation pathway, created by expanding the substrate scope of the carboxylic acid reductase toward noncognate ω-hydroxylic acids. Using the established platform as gateways, seven different diol-convertible amino acids are converted to diols including 1,3-propanediol, 1,4-butanediol, and 1,5-pentanediol. Particularly, we afford to optimize the production of 1,4-butanediol and demonstrate the de novo production of 1,5-pentanediol from glucose, with titers reaching 1.41 and 0.97 g l-1, respectively. Our work presents a metabolic platform that enriches the pathway repertoire for nonnatural diols with feedstock flexibility to both sugar and protein hydrolysates.Synthetic lethality strategies for cancer therapy exploit cancer-specific genetic defects to identify targets that are uniquely essential to the survival of tumor cells. Here we show RAD27/FEN1, which encodes flap endonuclease 1 (FEN1), a structure-specific nuclease with roles in DNA replication and repair, and has the greatest number of synthetic lethal interactions with Saccharomyces cerevisiae genome instability genes, is a druggable target for an inhibitor-based approach to kill cancers with defects in homologous recombination (HR). The vulnerability of cancers with HR defects to FEN1 loss was validated by studies showing that small-molecule FEN1 inhibitors and FEN1 small interfering RNAs (siRNAs) selectively killed BRCA1- and BRCA2-defective human cell lines. Furthermore, the differential sensitivity to FEN1 inhibition was recapitulated in mice, where a small-molecule FEN1 inhibitor reduced the growth of tumors established from drug-sensitive but not drug-resistant cancer cell lines. FEN1 inhibition induced a DNA damage response in both sensitive and resistant cell lines; however, sensitive cell lines were unable to recover and replicate DNA even when the inhibitor was removed.
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