Sweat excretion is a dynamic physiological process that varies with body position, activity level, environmental factors, and health status. Conventional means for measuring the properties of sweat yield accurate results but their requirements for sampling and analytics do not allow for use in the field. Emerging wearable devices offer significant advantages over existing approaches, but each has significant drawbacks associated with bulk and weight, inability to quantify volumetric sweat rate and loss, robustness, and/or inadequate accuracy in biochemical analysis. This paper presents a thin, miniaturized, skin‐interfaced microfluidic technology that includes a reusable, battery‐free electronics module for measuring sweat conductivity and rate in real‐time using wireless power from and data communication to electronic devices with capabilities in near field communications (NFC), including most smartphones. The platform exploits ultrathin electrodes integrated within a collection of microchannels as interfaces to circuits that leverage NFC protocols. The resulting capabilities are complementary to those of previously reported colorimetric strategies. Systematic studies of these combined microfluidic/electronic systems, accurate correlations of measurements performed with them to those of laboratory standard instrumentation, and field tests on human subjects exercising and at rest establish the key operational features and their utility in sweat analytics.

Through the formation of an electron donor–acceptor (EDA) complex, strain‐release aminopyridylation of [1.1.1]propellane with N‐aminopyridinium salts as bifunctional reagents enabled the direct installation of amino and pyridyl groups onto bicyclo[1.1.1]pentane (BCP) frameworks in the absence of an external photocatalyst. The robustness of this method to synthesize 1,3‐aminopyridylated BCPs under mild and metal‐free conditions is highlighted by the late‐stage modification of structurally complex biorelevant molecules. Moreover, the strategy was extended to P‐centered and CF3 radicals for the unprecedented incorporation of such functional groups with pyridine across the BCP core in a three‐component coupling. This practical method lays the foundation for the straightforward construction of new valuable C4‐pyridine‐functionalized BCP chemical entities, thus significantly expanding the range of accessibility of BCP‐type bioisosteres for applications in drug discovery.

This paper examines the impacts of the quality of government on international tourism competitiveness. Quality of government is conceptualized in terms of an absence of corruption, a well-established rule of law and bureaucratic efficiency. Based on the cross-country analysis of the Travel & Tourism Competitiveness Index (World Economic Forum, 2013), the main finding of the study demonstrates that quality of government is positively associated with tourism competitiveness and that this positive effect remains robust across a number of control variables and estimation techniques. The results suggest that public policy for building a successful tourism industry should be nested in the broader project of enhancing the quality of government.

A general strategy for visible‐light‐enabled site‐selective trifluoromethylative pyridylation of unactivated alkenes has been developed using pyridines and triflic anhydride (Tf2O). Intriguingly, the N‐triflylpyridinium salts, generated in situ from pyridines and Tf2O, serve as effective modular bifunctional reagents to install both CF3 and pyridyl groups to various olefins while controlling C4‐selectivity in radical addition to the pyridine core. This synthetic route exhibited broad substrate scope under metal‐free and mild photocatalytic conditions, granting efficient access to valuable C4‐alkylated pyridines and quinolines without requiring prefunctionalization of the reaction site.

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Background and purpose Progressive supranuclear palsy (PSP) encompasses a broader range of disease courses than previously appreciated. The most frequent clinical presentations of PSP are Richardson syndrome (RS) and PSP with a predominant Parkinsonism phenotype (PSP‐P). Time to reach gait dependence and cognitive impairment have been proposed as prognostic disease milestones. Genetic polymorphisms in TRIM11 and SLC2A13 genes have been associated with longer disease duration (DD). Methods Methods used include retrospective chart review, genetic single nucleotide polymorphism analyses (in three cases), and neuropathology. Results We identified four cases with long (>10–15 years) or very long (>15 years) DD. Stage 1 PSP tau pathology was present in two cases (one PSP‐P and one undifferentiated phenotype), whereas pallidonigroluysian atrophy (PSP‐RS) and Stage 4/6 (PSP‐P) PSP pathology were found in the other two cases. Three cases were homozygous for the rs564309‐C allele of the TRIM11 gene and the H1 MAPT haplotype. Two were heterozygous for rs2242367 (G/A) in SLC2A13, whereas the third was homozygous for the G‐allele. Conclusions We propose a protracted course subtype of PSP (PC‐PSP) based on clinical or neuropathological criteria in two cases with anatomically restricted PSP pathology, and very long DD and slower clinical progression in the other two cases. The presence of the rs564309‐C allele may influence the protracted disease course. Crystallizing the concept of PC‐PSP is important to further understand the pathobiology of tauopathies in line with current hypotheses of protein misfolding, seeding activity, and propagation.

Objective Progressive supranuclear palsy (PSP) is a 4R‐tauopathy showing heterogeneous tau cytopathology commencing in the globus pallidus (GP) and the substantia nigra (SN), regions also associated with age‐related iron accumulation. Abnormal iron levels have been extensively associated with tau pathology in neurodegenerative brains, however, its role in PSP pathogenesis remains yet unknown. We perform the first cell type‐specific evaluation of PSP iron homeostasis and the closely related oxygen homeostasis, in relation to tau pathology in human postmortem PSP brains. Methods In brain regions vulnerable to PSP pathology (GP, SN, and putamen), we visualized iron deposition in tau‐affected and unaffected neurons, astroglia, oligodendrocytes, and microglia, using a combination of iron staining with immunolabelling. To further explore molecular pathways underlying our observations, we examined the expression of key iron and oxygen homeostasis mRNA transcripts and proteins. Results We found astrocytes as the major cell type accumulating iron in the early affected regions of PSP, highly associated with cellular tau pathology. The same regions are affected by dysregulated expression of alpha and beta hemoglobin and neuroglobin showing contrasting patterns. We discovered changes in iron and oxygen homeostasis‐related gene expression associated with aging of the brain, and identified dysregulated expression of rare neurodegeneration with brain iron accumulation (NBIA) genes associated with tau pathology to distinguish PSP from the healthy aging brain. Interpretation We present novel aspects of PSP pathophysiology highlighting an overlap with NBIA pathways. Our findings reveal potential novel targets for therapy development and have implications beyond PSP for other iron‐associated neurodegenerative diseases. ANN NEUROL 2023;93:431–445

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