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Objective Obesity has traditionally been considered a risk factor for ischemic stroke. However, some clinical observations have reported a complex relationship between patients who are overweight or obese with paradoxically better stroke outcomes. Stroke subtypes have differing distributions of risk factors, so this study aimed to explain the relationship between body mass index (BMI) and functional prognosis according to stroke subtype. Methods A prospective institutional database on stroke was accessed between March 2014 and December 2021, and consecutive patients with ischemic stroke were retrospectively selected. BMI was categorized into five groups (underweight, normal weight, overweight, obese, and morbid obesity). The outcome of interest in this study was the modified Rankin Scale (mRS) at 90 d, which was divided into favorable (mRS = 0–2) and unfavorable (mRS ≥ 3) groups. The relationship between functional outcome and BMI was analyzed according to stroke subtype. Results Among 2779 patients with stroke, 913 (32.9%) had unfavorable outcomes. After a propensity score-matched analysis, obesity was inversely associated with unfavorable outcomes (adjusted odds ratio [aOR] = 0.61, 95% confidence interval [95% CI]: 0.46–0.80) in all patients with stroke. Among the stroke subtypes, overweight (aOR = 0.38, 95% CI: 0.20–0.74) and obese (aOR = 0.40, 95% CI: 0.21–0.76) groups were inversely associated with unfavorable outcomes in the cardioembolism subtype. Obesity (aOR = 0.55, 95% CI: 0.32–0.95) was inversely associated with unfavorable outcomes in the small vessel disease subtype. There was no significant relationship between stroke outcome and BMI classification in the large artery disease subtype. Conclusions These findings suggest that the obesity paradox in ischemic stroke outcomes might differ according to the stroke subtype.

Pupillometry, thanks to its strong relationship with cognitive factors and recent advancements in measuring techniques, has become popular among cognitive or neural scientists as a tool for studying the physiological processes involved in mental or neural processes. Despite this growing popularity of pupillometry, the methodological understanding of pupillometry is limited, especially regarding potential factors that may threaten pupillary measurements’ validity. Eye blinking can be a factor because it frequently occurs in a manner dependent on many cognitive components and induces a pulse-like pupillary change consisting of constriction and dilation with substantive magnitude and length. We set out to characterize the basic properties of this “blink-locked pupillary response (BPR),” including the shape and magnitude of BPR and their variability across subjects and blinks, as the first step of studying the confounding nature of eye blinking. Then, we demonstrated how the dependency of eye blinking on cognitive factors could confound, via BPR, the pupillary responses that are supposed to reflect the cognitive states of interest. By building a statistical model of how the confounding effects of eye blinking occur, we proposed a probabilistic-inference algorithm of de-confounding raw pupillary measurements and showed that the proposed algorithm selectively removed BPR and enhanced the statistical power of pupillometry experiments. Our findings call for attention to the presence and confounding nature of BPR in pupillometry. The algorithm we developed here can be used as an effective remedy for the confounding effects of BPR on pupillometry.

Carcinogenesis involves the chemical and structural alteration of biomolecules in cells. Aberrant methylation of DNA is a well-known carcinogenic mechanism and a common chemical modification of DNA. Terahertz waves can directly observe changes in DNA because the characteristic energies lie in the same frequency region. In addition, terahertz energy levels are not high enough to damage DNA by ionization. Here, we present terahertz molecular resonance fingerprints of DNA methylation in cancer DNA. Methylated cytidine, a nucleoside, has terahertz characteristic energies that give rise to the molecular resonance of methylation in DNA. Molecular resonance is monitored in aqueous solutions of genomic DNA from cancer cell lines using a terahertz time-domain spectroscopic technique. Resonance signals can be quantified to identify the types of cancer cells with a certain degree of DNA methylation. These measurements reveal the existence of molecular resonance fingerprints of cancer DNAs in the terahertz region, which can be utilized for the early diagnosis of cancer cells at the molecular level.

The skin serves as a complex barrier organ populated by tissue-resident macrophages (TRMs), which play critical roles in defense, homeostasis, and tissue repair. This review examines the functions of dermis resident TRMs in different inflammatory settings, their embryonic origins, and their long-term self-renewal capabilities. We highlight the M2-like phenotype of dermal TRMs and their specialized functions in perivascular and perineuronal niches. Their interactions with type 2 immune cells, autocrine cytokines such as IL-10, and their phagocytic clearance of apoptotic cells have been explored as mechanisms for M2-like dermal TRM self-maintenance and function. In conclusion, we address the need to bridge murine models with human studies, with the possibility of targeting TRMs to promote skin immunity or restrain cutaneous pathology. Bridging murine models to humans: targeting TRMs for skin immunity Our skin is more than just a physical shield; it’s a complex immune organ, filled with specialized cells like macrophages. In a detailed review, researchers explore these macrophages, focusing on their adaptability and function maintenance in the skin. This study synthesizes findings how macrophages interact with other immune cells, respond to inflammatory triggers, and contribute to tissue repair and homeostasis. The findings show that these macrophages can remain anti-inflammatory, even when faced with infections that usually trigger a strong immune response. They achieve this through various mechanisms, including interactions with specific immune cells that support their anti-inflammatory state, and engaging in processes that promote tissue repair without increasing inflammation. The researchers conclude that understanding these mechanisms opens new possibilities for treating skin diseases by targeting or mimicking the ways these macrophages control inflammation and support healing. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.

Our perception is often attracted to what we have seen before, a phenomenon called ‘serial dependence.’ Serial dependence can help maintain a stable perception of the world, given the statistical regularity in the environment. If serial dependence serves this presumed utility, it should be pronounced when consecutive elements share the same identity when multiple elements spatially shift across successive views. However, such preferential serial dependence between identity-matching elements in dynamic situations has never been empirically tested. Here, we hypothesized that serial dependence between consecutive elements is modulated more effectively by the spatial correspondence in relative space than by that in absolute space because spatial correspondence in relative coordinates can warrant identity matching invariantly to changes in absolute coordinates. To test this hypothesis, we developed a task where two targets change positions in unison between successive views. We found that serial dependence was substantially modulated by the correspondence in relative coordinates, but not by that in absolute coordinates. Moreover, such selective modulation by the correspondence in relative space was also observed even for the serial dependence defined by previous non-target elements. Our findings are consistent with the view that serial dependence subserves object-based perceptual stabilization over time in dynamic situations.

The environmental impacts of mine dust in mining operations can be mitigated through improved prediction of its spatial distribution using dispersion models, particularly Gaussian-based air quality models. However, Gaussian-based models often predict concentrations that differ substantially from observed mine dust behavior, because dust properties and transport mechanisms vary markedly with particle size. In this study, particle-size-related mechanisms for dust dispersion behaviors were classified as dry/wet deposition, turbulent diffusivity, erosion, hygroscopicity, or agglomeration, and their effects on dust dispersion behaviors and effective simulation methods were reviewed. Currently, the most clearly established particle size influence is on deposition, especially for coarse dust emitted from mechanical mining processes. Other mechanisms, including erosion, hygroscopicity, and agglomeration, are more relevant to finer dust below 2.5 µm or in the submicron range. This study proposes that wind erosion, mainly saltation flux, can also be integrated into Gaussian dispersion models as near-ground boundary flux terms. Hygroscopic and agglomeration effects can be assessed using relative humidity and simplified particle size redistribution assumptions near dust emission sources. In particular, incorporation of agglomeration mechanisms may begin with a simple bimodal assumption: the agglomeration of PM2.5 into PM10. This can be incorporated into a modified Gaussian deposition equation. Finally, the size dependence of the turbulent diffusivity coefficient is relatively insignificant, so the diffusivity values can be regarded as constants. These findings provide a mechanistic basis for improving mine dust prediction and environmental management in open-pit mines, haul roads, tailings areas, and stockpile environments.

Astrocytes and microglia are brain‐resident glia that can establish harmful inflammatory environments in disease contexts and thereby contribute to the progression of neuronal loss in neurodegenerative disorders. Correcting the diseased properties of glia is therefore an appealing strategy for treating brain diseases. Previous studies have shown that serum/ glucocorticoid related kinase 1 (SGK1) is upregulated in the brains of patients with various neurodegenerative disorders, suggesting its involvement in the pathogenesis of those diseases. In this study, we show that inhibiting glial SGK1 corrects the pro‐inflammatory properties of glia by suppressing the intracellular NFκB‐, NLRP3‐inflammasome‐, and CGAS‐STING‐mediated inflammatory pathways. Furthermore, SGK1 inhibition potentiated glial activity to scavenge glutamate toxicity and prevented glial cell senescence and mitochondrial damage, which have recently been reported as critical pathologic features of and therapeutic targets in Parkinson disease (PD) and Alzheimer disease (AD). Along with those anti‐inflammatory/neurotrophic functions, silencing and pharmacological inhibition of SGK1 protected midbrain dopamine neurons from degeneration and cured pathologic synuclein alpha (SNCA) aggregation and PD‐associated behavioral deficits in multiple in vitro and in vivo PD models. Collectively, these findings suggest that SGK1 inhibition could be a useful strategy for treating PD and other neurodegenerative disorders that share the common pathology of glia‐mediated neuroinflammation. Synopsis Pathogenic involvement of SGK1 has been implicated in various neurodegenerative disorders. In this study, we show that inhibition of SGK1 in glia treats Parkinson disease (PD) via suppressing glial inflammation and potentiating glial neurotrophic functions. SGK inhibition reduces neuroinflammation and protects dopamine neurons from degeneration. PD – associated behavioral deficits are improved in PD mice after SGK inhibition. Inhibition of SGK1 could be a useful strategy for treating PD and other neurodegenerative disorders. Graphical Abstract Pathogenic involvement of SGK1 has been implicated in various neurodegenerative disorders. In this study, we show that inhibition of SGK1 in glia treats Parkinson disease (PD) via suppressing glial inflammation and potentiating glial neurotrophic functions.

The dipole characteristics of Frenkel excitons and charge-transfer excitons between donor and acceptor molecules in organic heterostructures such as exciplexes are important in organic photonics and optoelectronics. For the bilayer of the organic donor 4,4′,4′′-tris[(3-methylphenyl)phenylamino]triphenylamine and acceptor 2,4,6-tris(biphenyl-3-yl)-1,3,5-triazine molecules, the exciplexes form aligned dipoles perpendicular to the Frenkel excitons, as observed in back focal plane photoluminescence images. The angular chromism of exciplexes observed in the 100 meV range indicates possible delocalization and angle-sensing photonic applications. The blue shift of the peak position and increase in the linewidth of photoluminescene spectra with increasing excitation power are caused by the repulsive aligned exciplex dipole moments with a long lifetime (4.65 μs). Electroluminescence spectra of the exciplex from organic light-emitting diodes using the bilayer are blue-shifted with increasing bias, suggesting unidirectional alignment of the exciplex dipole moments. The observation of exciplex dipole moment alignments across molecular interfaces can facilitate the controlled coupling of exciton species and increase efficiency of organic light-emitting diodes. The directional features of dipole moments of Frenkel excitons and exciplexes are important for optoelectronic applications. Here, the authors study photo- and electro-luminescence emissions of organic heterostructures and observe angular chromism of exciplexes, indicating possible delocalization.

Autophagy is an intracellular degradative process that occurs under several stressful conditions, including organelle damage, the presence of abnormal proteins, and nutrient deprivation. The mechanism of autophagy initiates the formation of autophagosomes that capture degraded components and then fuse with lysosomes to recycle these components. The modulation of autophagy plays dual roles in tumor suppression and promotion in many cancers. In addition, autophagy regulates the properties of cancer stem-cells by contributing to the maintenance of stemness, the induction of recurrence, and the development of resistance to anticancer reagents. Although some autophagy modulators, such as rapamycin and chloroquine, are used to regulate autophagy in anticancer therapy, since this process also plays roles in both tumor suppression and promotion, the precise mechanism of autophagy in cancer requires further study. In this review, we will summarize the mechanism of autophagy under stressful conditions and its roles in tumor suppression and promotion in cancer and in cancer stem-cells. Furthermore, we discuss how autophagy is a promising potential therapeutic target in cancer treatment.

Despite limited information and knowledge, we personally form beliefs about certain properties of objects encountered in our daily life-popularity of a newly released movie, for example. Since such beliefs are prone to error, we often revise our initial beliefs according to the beliefs of others to improve accuracy. Optimal revision requires modulating the degree of accepting others' beliefs based on various cues for accuracy-number of opinions, for example-such that the more accurate others' beliefs are, the more we accept them. Although previous studies have shown that such accuracy cues can influence the degree of acceptance during social revision, they primarily investigated problems with 'factually correct' answers, and rarely problems with 'socially correct' answers. Here we examined which accuracy cues are objectively useful (utility of cues), and how those cues are used (use of cues), in the social revision of people's beliefs about problems with 'socially correct' answers. We asked people to estimate the 'shared preferences (SPs)' for sociocultural items, the answers to which are determined by socially aggregated beliefs-how popular an abstract painting will be among a large crowd, for example-and then to revise their initial estimates after being exposed to other people's estimates about the same items. We considered 'confidence', 'agreement among estimates', and 'number of estimates' as accuracy cues. We found that, while all three cues validly signaled the accuracy of SP estimates, only the 'number' cue has a significant utility, but the other cues are much less useful for optimal revision. Nevertheless, people used the cues of 'agreement' and their own 'confidence' to the extent comparable to that of the 'number' cue. Our findings suggest that the utility and use of accuracy cues for problems with 'socially correct' answers differ from those with 'factually correct' answers, as follows: (i) confidence does not have a significant utility and (ii) but people use their own confidence while ignoring others' confidence.