Emerging evidence implicates organelle dysfunction, particularly within peroxisomes, as a critical driver of hair follicle degeneration and alopecia. While mitochondrial defects are well characterized in the context of hair loss, the contribution of peroxisomal failure to follicular homeostasis remains largely unexplored. Here, we identify peroxisomal dysfunction as a central molecular and metabolic defect underlying hair follicle aging and loss. Comprehensive transcriptomic analysis of human dermal papilla cells from alopecia patients revealed marked downregulation of peroxisome-associated pathways, including fatty acid β-oxidation, lipid degradation, and detoxification of reactive oxygen species. These alterations were recapitulated in <i>Nudt7</i>-deficient mice, in which targeted disruption of peroxisomal lipid metabolism leads to pronounced hair thinning, follicle miniaturization, and exacerbated oxidative stress. To therapeutically address peroxisomal impairment, we developed catalytic nanozymes (HA-Hem) that mimic peroxisomal catalase activity. Nanozyme treatment restored metabolic balance, reduced oxidative damage, and stimulated hair follicle regeneration in both wild-type and immunodeficient murine models. Mechanistically, nanozymes increased PPARα expression, thereby enhancing peroxisomal biogenesis and lipid metabolism. Elevated PPARα further improved peroxisome and mitochondrial function and strengthened peroxisome-mitochondria interactions, resulting in coordinated restoration of cellular redox and metabolic homeostasis. Compared with minoxidil treatment, nanozyme therapy produced greater regenerative responses and maintained therapeutic efficacy in immunodeficient settings. Spatial transcriptomic analysis further demonstrated an increased expression of keratin-associated proteins and cytoskeletal genes, consistent with activation of regenerative programs. These findings support a metabolism-focused therapeutic strategy targeting peroxisomal function in the treatment of alopecia.

Emerging evidence implicates organelle dysfunction, particularly within peroxisomes, as a critical driver of hair follicle degeneration and alopecia. While mitochondrial defects are well characterized in the context of hair loss, the contribution of peroxisomal failure to follicular homeostasis remains largely unexplored. Here, we identify peroxisomal dysfunction as a central molecular and metabolic defect underlying hair follicle aging and loss. Comprehensive transcriptomic analysis of human dermal papilla cells from alopecia patients revealed marked downregulation of peroxisome-associated pathways, including fatty acid β-oxidation, lipid degradation, and detoxification of reactive oxygen species. These alterations were recapitulated in <i>Nudt7</i>-deficient mice, in which targeted disruption of peroxisomal lipid metabolism leads to pronounced hair thinning, follicle miniaturization, and exacerbated oxidative stress. To therapeutically address peroxisomal impairment, we developed catalytic nanozymes (HA-Hem) that mimic peroxisomal catalase activity. Nanozyme treatment restored metabolic balance, reduced oxidative damage, and stimulated hair follicle regeneration in both wild-type and immunodeficient murine models. Mechanistically, nanozymes increased PPARα expression, thereby enhancing peroxisomal biogenesis and lipid metabolism. Elevated PPARα further improved peroxisome and mitochondrial function and strengthened peroxisome-mitochondria interactions, resulting in coordinated restoration of cellular redox and metabolic homeostasis. Compared with minoxidil treatment, nanozyme therapy produced greater regenerative responses and maintained therapeutic efficacy in immunodeficient settings. Spatial transcriptomic analysis further demonstrated an increased expression of keratin-associated proteins and cytoskeletal genes, consistent with activation of regenerative programs. These findings support a metabolism-focused therapeutic strategy targeting peroxisomal function in the treatment of alopecia.

Osteoarthritis (OA) is a long-term degenerative condition of the joints, characterized by persistent inflammation, progressive cartilage breakdown, and impaired mitochondrial function. Recent studies have shown that hyperactivation of the mTORC1 pathway and metabolic reprogramming of chondrocytes contribute to disease progression. Nitazoxanide (NTZ), an oral antiparasitic agent approved by the Food and Drug Administration, has shown anti-inflammatory and mitochondrial protective effects in various disease situations; despite this, its application in osteoarthritis has yet to be fully investigated. Here, we assessed the therapeutic efficacy of NTZ using IL-1β-stimulated primary chondrocytes derived from patients with OA. NTZ substantially reduced the expression of proinflammatory cytokines and matrix metalloproteinases, restored mitochondrial membrane potential, and reduced mitochondrial reactive oxygen species levels. NTZ also effectively reversed IL-1β-induced glycolytic metabolic changes by inhibiting glucose uptake and GLUT1 expression. Mechanistically, NTZ inhibited the activation of the mTORC1 pathway and substantially increased AMPK phosphorylation. The siRNA-mediated AMPK knockdown negated NTZ-induced mitochondrial and metabolic improvements, suggesting that AMPK is a key upstream regulator of the protective actions of NTZ. NTZ can, therefore, effectively inhibit inflammatory metabolic reprogramming and mitochondrial dysfunction in OA chondrocytes through AMPK-dependent mTORC1 signaling inhibition, highlighting its potential as a disease-modifying therapy for OA.

In this article, we investigate the effect of annealing in deuterium (D2) ambient on the performance and reliability of InGaZnO (IGZO) thin-film transistors (TFTs). We examined the current-voltage (I–V) characteristics, as well as the on-state current (<inline-formula xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink"> <tex-math notation="LaTeX">$I_{\text{on}}$ </tex-math></inline-formula>), off-state current (<inline-formula xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink"> <tex-math notation="LaTeX">$I_{\text{off}}$ </tex-math></inline-formula>), and subthreshold slope (SS) under three different conditions: after device fabrication (as-fabricated), in a deteriorated state (after 7 days), and after D2 annealing. To analyze the reliability of IGZO TFTs, the oxygen vacancy (<inline-formula xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink"> <tex-math notation="LaTeX">$V_{\text{O}}$ </tex-math></inline-formula>) behavior was observed by extracting the subgap density of state (DOS) using I–V data. Quantitative and qualitative analyses of the changes in ion distribution inside the IGZO channel after D2 annealing were performed by X-ray photoelectron spectroscopy (XPS) and secondary-ion mass spectrometry (SIMS), respectively, both of which verified the effect of the D2 annealing. The validity of our results was further verified by comparing them to model parameters generated using a technology computer-aided design (TCAD) simulation.

Abstract As CMOS technology continues to advance and scale down, conventional post-metallization annealing (PMA), conducted to enhance yield and device performance, needs to evolve due to its excessively high thermal stress and long duration. In this context, this study proposes rapid deuterium annealing (RDA) as an alternative to conventional PMA for minimizing the thermal budget. Compared to conventional PMA, the RDA process shortened the annealing time from 30 min to 3 min, thereby effectively reducing the thermal budget. High- k metal gate MOSFETs are fabricated for process verification, and the impact of RDA is investigated through device characterization. After the RDA process, device performance and stress immunity have been enhanced through passivation of interface traps.

Wearable devices, such as actigraphy monitors and continuous glucose monitors (CGMs), capture high-frequency data, which are often summarized by the percentages of time spent within fixed thresholds. For example, actigraphy data are categorized into sedentary, light, and moderate-to-vigorous activity, while CGM data are divided into hypoglycemia, normoglycemia, and hyperglycemia based on a standard glucose range of $70\text{unicode}x2013180$ mg/dL. Although scientific and clinical guidelines inform the choice of thresholds, it remains unclear whether this choice is optimal and whether the same thresholds should be applied across different populations. In this work, we define threshold optimality with loss functions that quantify discrepancies between the full empirical distributions of wearable device measurements and their discretizations based on specific thresholds. We introduce two loss functions: one that aims to accurately reconstruct the original distributions and another that preserves the pairwise sample distances. Using the Wasserstein distance as the base measure, we reformulate the loss minimization as optimal piecewise linearization of quantile functions. We solve this optimization via stepwise algorithms and differential evolution. We also formulate semi-supervised approaches where some thresholds are predefined based on scientific rationale. Applications to CGM data from two distinct populations$\text{unicode}x2014$individuals with type 1 diabetes and those with normal glycemic control$\text{unicode}x2014$demonstrate that data-driven thresholds vary by population and improve discriminative power over fixed thresholds.

증가하는 수요와 다양한 환경의 무선 네트워크에서는 충돌, 지연, 공정성, 전력 소모 등과 같은 많은 문제들이 발행하고 있다. 이러한 문제들을 인공지능 기술을 활용하여 해결하거나 최소화시켜 프로토콜의 성능을 향상시키는 연구들이 논의되고 있다. 본 논문에서는 무선 네트워크 환경의 MAC 프로토콜에서 위에서 서술한 문제를 해결하기 위해 강화 학습 기술을 사용한 연구들에 대해서 조사했다. 무선 네트워크 MAC 프로토콜에서 나타나는 문제점을 살펴보고, 강화 학습이 어떻게 활용되었는지 알아본다. 마지막으로 향후 해결해야 하는 문제점을 서술한다