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Shaping single-mode operation in high-power fibers requires a precise knowledge of the gain-medium optical properties. This requires precise measurements of the refractive index differences (Δ n ) between the core and the cladding of the fiber. We exploit a quantum optical method based on low-coherence Hong-Ou-Mandel interferometry to perform practical measurements of the refractive index difference using broadband energy-time entangled photons. The precision enhancement reached with this method is benchmarked with a classical method based on single photon interferometry. We show in classical regime an improvement by an order of magnitude of the precision compared to already reported classical methods. Strikingly, in the quantum regime, we demonstrate an extra factor of 4 on the precision enhancement, exhibiting a state-of-the-art Δ n precision of 6 × 10 −7 . This work sets the quantum photonics metrology as a powerful characterization tool that should enable a faster and reliable design of materials dedicated to light amplification.

We report a novel and highly sensitive torsion sensor that integrates a multicore fiber (MCF) within a Sagnac interferometer so that the same MCF segment serves as both the reflective element and the sensing head of a fiber-ring laser. The laser architecture incorporates a distributed reflector implemented as a ZnGa₂O₄-nanocrystal-doped fiber section, which enhances overall system performance. The device exhibits high torsional responsivity over 0°–150°, with distinct behavior across sub-ranges: in 0°–50°, phase analysis yields a sensitivity of 0.08 rad/° with R² = 0.991; in 88°–150°, amplitude analysis—under the ring-laser configuration—shows an improvement in sensitivity from 0.2 to 0.5 dBm/° (R² = 0.995). In the intermediate interval (50°–88°) neither phase nor power varies monotonically, so a function-fitting neural network was employed to bridge this gap, achieving a root-mean-square error of 0.06°. The system attains an angular resolution of 0.8°, ensuring accurate torsion estimation across the entire measurement span.

While excessive production of reactive oxygen species (ROS) is a characteristic hallmark of numerous diseases, clinical approaches that ameliorate oxidative stress have been unsuccessful. Here, utilizing multi-omics, we demonstrate that in cardiomyocytes, mitochondrial isocitrate dehydrogenase (IDH2) constitutes a major antioxidative defense mechanism. Paradoxically reduced expression of IDH2 associated with ventricular eccentric hypertrophy is counterbalanced by an increase in the enzyme activity. We unveil redox-dependent sex dimorphism, and extensive mutual regulation of the antioxidative activities of IDH2 and NRF2 by a feedforward network that involves 2-oxoglutarate and L-2-hydroxyglutarate and mediated in part through unconventional hydroxy-methylation of cytosine residues present in introns. Consequently, conditional targeting of ROS in a murine model of heart failure improves cardiac function in sex- and phenotype-dependent manners. Together, these insights may explain why previous attempts to treat heart failure with antioxidants have been unsuccessful and open new approaches to personalizing and, thereby, improving such treatment. Efforts to treat heart failure with antioxidants have failed. Here, authors reveal a robust sex-dependent endogenous defense against oxidative damage and demonstrate antioxidative treatment’s efficacy solely in subjects with inadequate redox capacity.

Background: Delirium frequently affects older emergency department (ED) patients and has been associated with accelerated cognitive and functional decline, increased length of stay (LOS), and higher in- and out-of-hospital mortality. Objectives: Care provided in the ED may have downstream effects on delirium duration during hospitalization. This study aimed to identify the modifiable factors of ED care associated with delirium duration in patients admitted to the hospital through the ED. Materials and Methods: This prospective cohort study enrolled ED patients who were 65 years and older and admitted to the hospital. Delirium was determined in the ED and during the first 7 days of hospitalization using the modified Brief Confusion Assessment Method. All delirious patients and a random selection (17%) of nondelirious patients were also enrolled. ED LOS, opioid administration, benzodiazepine administration, anticholinergic medication administration, and bladder catheter placement were obtained by medical record review. Multivariable proportional odds logistic regression was performed to determine if each of the factors was associated with delirium duration after adjusting for age, dementia, baseline function, comorbidity burden, severity of illness, nursing home residence, and central nervous system insult. Results: A total of 228 patients were enrolled. ED bladder catheter placement was significantly associated (adjusted proportional odds ratio = 3.1, 95% confidence interval: 1.3 to 7.4) with increased delirium duration after adjusting for confounders. ED LOS, opioid administration, benzodiazepine administration, and anticholinergic burden, however, were not. Conclusions: ED bladder catheter placement was significantly associated with delirium duration and may present an opportunity for intervention.

Excessive production of reactive oxygen species (ROS) is characteristic of numerous diseases, but most studies in this area have not considered the impact of endogenous antioxidative defenses. Here, utilizing multi-omics, we demonstrate that in cardiomyocytes mitochondrial isocitrate dehydrogenase (IDH2) constitutes a major antioxidant defense. In both male and female mice and humans the paradoxical reduction in expression of IDH2 associated with heart failure is compensated for by an increase in the enzyme's activity. We describe extensive mutual regulation of the antioxidant activities of IDH2 and NRF2 by a network involving 2-oxoglutarate and L2-hydroxyglutarate and mediated in part through unconventional hydroxymethylation of cytosine residues present in introns. Conditional targeting of ROS in a murine model of heart failure improves cardiac function. Together, these insights may explain why previous attempts to treat heart failure with antioxidants have been unsuccessful and open new approaches to personalizing and, thereby, improving such treatment. Competing Interest Statement The authors have declared no competing interest.