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The vertical deposition technique and the RF-magnetron sputtering method were employed for fabrication of three-dimensional (3-D) magnetophotonic crystals, in which a bismuth-substituted yttrium-iron-garnet planar defect layer was sandwiched in between two opal thin films. Optical properties and structure of constitutive elements (opal thin films) were studied in detail. An evolution of optical response of a magnetophotonic heterostructure under preparation is presented. Index Terms--Heterostructure, magnetophotonic crystal.

We report results on fabrication of three-dimensional (3D)-magnetophotonic crystals (MPCs) based on artificial opals. The opal samples composed of amorphous Si[O.sub.2] spheres were prepared using gravitational sedimentation. Quantitative evaluation of opal structure was done by fitting the (111) photonic bandgap by a Gaussian function. Changes in depth and width of the (111) photonic bandgap were observed after polishing less-ordered bottom side of the as-grown opal samples. To create 3D-MPCs, terbium gallium garnet was synthesized in an opal matrix. Index Terms--Artificial opal, magnetophotonic crystal (MPC), photonic crystal, sedimentation.

The optical and magneto-optical properties of bismuth-substituted yttrium iron garnet (Bi:YIG) films with Au nanoparticles dispersed on their top surfaces are studied. Polarization-resolved transmission spectra have shown that the rotation is due to anisotropy of light propagation through the array of Au nanoparticles.

X-ray diffraction analysis was used to study the structure of Fe97− x Zr3N x thin films produced under different conditions of rf magnetron sputtering (on rotary and stationary substrates) and subsequent annealing. Either a single-phase structure, namely, a supersaturated bcc α-(FeN) solid solution, or a mixed structure that consists of two crystalline phases, such as a supersaturated bcc α-Fe(N) solid solution and an fcc Fe4N nitride, and a Fe-based amorphous phase were shown to be formed in films deposited on either stationary or rotating substrate, respectively. As the annealing temperature increases, the content of nitrogen in the bcc phase decreases; the grain size of the bcc phase in the films deposited on rotating and stationary substrates increases from 8 to 14 nm and from 10 to 30 nm, respectively; the amount of the Fe4N phase increases. The results of the study of the magnetic properties of the films are reported. The maximum saturation induction B s reached is 1.8–1.9 T; the minimum coercive force H c is 1 Oe. The optimum combination of the magnetic properties ( B s = 1.8–1.9 T and H c = 1.5–1.8 Oe) is observed for the films deposited on the rotating substrate and subsequently annealed at 400°C. [ABSTRACT FROM AUTHOR]

Fe79Zr10N11 films 0.7 μm thick deposited on glass substrates have been produced by rf reactive magnetron sputtering. The films are a soft magnetic material, which can exhibit a combination of a high saturation inductance and a low coercive force and, therefore, shows promise as magnetic recording cores for the high-density magnetic recording. The results of X-ray diffraction studies of the phase and structural states of the films and the effect of annealing on these states are considered. [ABSTRACT FROM AUTHOR]

Recent studies have highlighted the potential involvement of reactive oxygen species (ROS) and microglia, a major source of ROS, in the pathophysiology of schizophrenia. In our study, we explored how the second-generation antipsychotic risperidone (RIS) affects ROS regulation and microglial activation in the hippocampus using a mouse ketamine (KET) model of schizophrenia. KET administration resulted in schizophrenia-like behaviors in male C57BL/6J mice, such as impaired prepulse inhibition (PPI) of the acoustic startle response and hyper-locomotion. These behaviors were mitigated by RIS. We found that the gene expression level of an enzyme responsible for ROS production (Nox2), which is primarily associated with activated microglia, was lower in KET/RIS-treated mice than in KET-treated mice. Conversely, the levels of antioxidant enzymes (Ho-1 and Gclc) were higher in KET/RIS-treated mice. The microglial density in the hippocampus was increased in KET-treated mice, which was counteracted by RIS. Hierarchical cluster analysis revealed three morphological subtypes of microglia. In control mice, most microglia were resting-ramified (type I, 89.7%). KET administration shifted the microglial composition to moderately ramified (type II, 44.4%) and hyper-ramified (type III, 25.0%). In KET/RIS-treated mice, type II decreased to 32.0%, while type III increased to 34.0%. An in vitro ROS assay showed that KET increased ROS production in dissociated hippocampal microglia, and this effect was mitigated by RIS. Furthermore, we discovered that a NOX2 inhibitor could counteract KET-induced behavioral deficits. These findings suggest that pharmacological inhibition of ROS production by RIS may play a crucial role in ameliorating schizophrenia-related symptoms. Moreover, modulating microglial activation to regulate ROS production has emerged as a novel avenue for developing innovative treatments for schizophrenia., (© 2024 International Society for Neurochemistry.)

Objective: To evaluate hemostatic efficacy, complications, and subsequent pregnancy outcomes in women with placenta previa who underwent combined vertical compression sutures in the lower uterine segment and intrauterine balloon tamponade (Hot-Dog method) to achieve hemostasis after cesarean section., Methods: We retrospectively reviewed data for 117 women with singleton pregnancy diagnosed with placenta previa who underwent cesarean section between 29 and 38 weeks' gestation. Treatments were as follows: (1) conventional-intravenous oxytocin administration after placental detachment and suturing of bleeding points at the detachment site as needed (conventional group) (n = 47). (2) Intrauterine balloon tamponade alone (balloon group) (n = 41). (3) Vertical compression sutures + intrauterine balloon tamponade (Hot-Dog group) (n = 29)., Results: The placenta accreta spectrum prevalence was significantly higher in the balloon and Hot-Dog groups versus the conventional group. The prevalence of anteriorly located placenta was significantly higher in the Hot-Dog versus balloon groups. Intraoperative and total blood loss were significantly higher in the Hot-Dog versus conventional groups. Postoperative blood loss was significantly lower in the Hot-Dog versus balloon groups. Fewer additional procedures for managing postoperative hemorrhage were required in the Hot-Dog versus conventional and balloon groups. The number of subsequent pregnancies in the conventional, balloon, and Hot-Dog groups was 11 (23.4%), 8 (19.5%), and 4 (13.8%), respectively; all resulted in live births at term without serious obstetric complications., Conclusion: The Hot-Dog method is a straightforward and safe hemostasis technique for placenta previa that preserves fertility and controls severe bleeding., (© 2024 The Author(s). International Journal of Gynecology & Obstetrics published by John Wiley & Sons Ltd on behalf of International Federation of Gynecology and Obstetrics.)

CD11c-positive (CD11c + ) microglia have attracted considerable attention because of their potential implications in central nervous system (CNS) development, homeostasis, and disease. However, the spatiotemporal dynamics of the proportion of CD11c + microglia in individual CNS regions are poorly understood. Here, we investigated the proportion of CD11c + microglia in six CNS regions (forebrain, olfactory bulb, diencephalon/midbrain, cerebellum, pons/medulla, and spinal cord) from the developmental to adult stages by flow cytometry and immunohistochemical analyses using a CD11c reporter transgenic mouse line, Itgax-Venus. We found that the proportion of CD11c + microglia in total microglia varied between CNS regions during postnatal development. Specifically, the proportion was high in the olfactory bulb and cerebellum at postnatal day P(4) and P7, respectively, and approximately half of the total microglia were CD11c + . The proportion declined sharply in all regions to P14, and the low percentage persisted over P56. In the spinal cord, the proportion of CD11c + microglia was also high at P4 and declined to P14, but increased again at P21 and thereafter. Interestingly, the distribution pattern of CD11c + microglia in the spinal cord markedly changed from gray matter at P4 to white matter at P21. Collectively, our findings reveal the differences in the spatiotemporal dynamics of the proportion of CD11c + microglia among CNS regions from early development to adult stages in normal mice. These findings improve our understanding of the nature of microglial heterogeneity and its dynamics in the CNS., (© 2024. The Author(s).)

Post-traumatic stress disorder (PTSD) is a hypermnesic condition that develops in a subset of individuals following exposure to severe trauma. PTSD symptoms are debilitating, and include increased anxiety, abnormal threat generalization, and impaired extinction. In developing treatment strategies for PTSD, preclinical studies in rodents have largely focused on interventions that target post-encoding memory processes such as reconsolidation and extinction. Instead, here we focus on forgetting, another post-encoding process that regulates memory expression. Using a double trauma murine model for PTSD, we asked whether promoting neurogenesis-mediated forgetting can weaken trauma memories and associated PTSD-relevant behavioral phenotypes. In the double trauma paradigm, consecutive aversive experiences lead to a constellation of behavioral phenotypes associated with PTSD including increases in anxiety-like behavior, abnormal threat generalization, and deficient extinction. We found that post-training interventions that elevate hippocampal neurogenesis weakened the original trauma memory and decreased these PTSD-relevant phenotypes. These effects were observed using multiple methods to manipulate hippocampal neurogenesis, including interventions restricted to neural progenitor cells that selectively promoted integration of adult-generated granule cells into hippocampal circuits. The same interventions also weakened cocaine place preference memories, suggesting that promoting hippocampal neurogenesis may represent a broadly useful approach in hypermnesic conditions such as PTSD and substance abuse disorders., (© 2024. The Author(s), under exclusive licence to Springer Nature Limited.)

Background/aim: There have been many studies on skeletal muscle depletion before surgery, and skeletal muscle depletion is a known risk factor for poor prognosis. However, reports on the association between changes in skeletal muscle mass and prognosis after surgery for pancreatic cancer are very few., Patients and Methods: The data of 137 patients who underwent pancreatectomy for pancreatic cancer between 2005 and 2022 were reviewed. Muscle areas were measured at the third lumbar vertebral level, and skeletal muscle mass index (SMI) reduction rates were calculated. Patients were divided into two groups using receiver operating characteristic (ROC) curve analysis based on the SMI reduction rate with a cutoff of 14% reduction rate. The clinicopathological factors, overall survival (OS), and recurrence-free survival (RFS) were compared between the two groups. Survival rates were analyzed both univariately and multivariately to clarify the factors associated with poor prognosis after pancreatectomy., Results: A total of 102 patients met the inclusion criteria. SMI reduction rate ≥14% significantly correlated with advanced age and higher incidence of postoperative complications. In the multivariate Cox regression analysis, preoperative prognostic nutritional index (PNI) <40 and SMI reduction rate ≥14% were significantly associated with poor OS. Tumor size ≥3.0 cm, preoperative neutrophile-lymphocyte ratio ≥3.0, and SMI reduction rate ≥14% were significantly associated with poor RFS., Conclusion: The rate of skeletal muscle mass reduction after pancreatic surgery is an independent prognostic factor for survival in patients with pancreatic cancer., Competing Interests: The Authors declare that they have no competing interests in relation to this study., (Copyright 2024, International Institute of Anticancer Research.)

Objectives: To clarify the impact of central nervous system (CNS) metastasis on performance status (PS) at relapse, on subsequent treatment(s), and on survival of patients with lung adenocarcinoma harboring common epidermal growth factor receptor (EGFR) mutation., Methods: We conducted the multicenter real-world database study for patients with radical resections for lung adenocarcinomas between 2015 and 2018 at 21 centers in Japan. EGFR mutational status was examined at each center., Results: Of 4181 patients enrolled, 1431 underwent complete anatomical resection for lung adenocarcinoma harboring common EGFR mutations. Three-hundred-and-twenty patients experienced disease relapse, and 78 (24%) had CNS metastasis. CNS metastasis was significantly more frequent in patients with conventional adjuvant chemotherapy than those without (30% vs. 20%, P = 0.036). Adjuvant chemotherapy did not significantly improve relapse-free survival at any pathological stage (adjusted hazard ratio for stage IA2-3, IB, and II-III was 1.363, 1.287, and 1.004, respectively). CNS metastasis did not affect PS at relapse. Subsequent treatment, mainly consisting of EGFR-tyrosine kinase inhibitors (TKIs), could be equally given in patients with or without CNS metastasis (96% vs. 94%). Overall survival after relapse was equivalent between patients with and without CNS metastasis., Conclusion: The efficacy of conventional adjuvant chemotherapy may be limited in patients with lung adenocarcinoma harboring EGFR mutations. CNS metastasis is likely to be found in practice before deterioration in PS, and may have little negative impact on compliance with subsequent EGFR-TKIs and survival after relapse. In this era of adjuvant TKI therapy, further prospective observational studies are desirable to elucidate the optimal management of CNS metastasis., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Neuroaxonal dystrophy (NAD) is a neurodegenerative disease characterized by spheroid (swollen axon) formation in the nervous system. In the present study, we focused on a newly established autosomal recessive mutant strain of F344- kk / kk rats with hind limb gait abnormalities and ataxia from a young age. Histopathologically, a number of axonal spheroids were observed throughout the central nervous system, including the spinal cord (mainly in the dorsal cord), brain stem, and cerebellum in F344- kk / kk rats. Transmission electron microscopic observation of the spinal cord revealed accumulation of electron-dense bodies, degenerated abnormal mitochondria, as well as membranous or tubular structures in the axonal spheroids. Based on these neuropathological findings, F344- kk / kk rats were diagnosed with NAD. By a positional cloning approach, we identified a missense mutation (V95E) in the Hspa8 (heat shock protein family A (Hsp70) member 8) gene located on chromosome 8 of the F344- kk / kk rat genome. Furthermore, we developed the Hspa8 knock-in (KI) rats with the V95E mutation using the CRISPR-Cas system. Homozygous Hspa8 -KI rats exhibited ataxia and axonal spheroids similar to those of F344- kk / kk rats. The V95E mutant HSC70 protein exhibited the significant but modest decrease in the maximum hydrolysis rate of ATPase when stimulated by co-chaperons DnaJB4 and BAG1 in vitro , which suggests the functional deficit in the V95E HSC70. Together, our findings provide the first evidence that the genetic alteration of the Hspa8 gene caused NAD in mammals., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Tanaka, Fujikawa, Sekiguchi, Hernandez, Johnson, Tanaka, Kumafuji, Serikawa, Hoang Trung, Hattori, Mashimo, Kuwamura, Gestwicki and Kuramoto.)

Understanding the principles of cell migration necessitates measurements of the forces generated by cells. In traction force microscopy (TFM), fluorescent beads are placed on a substrate's surface and the substrate strain caused by the cell traction force is observed as displacement of the beads. Mathematical analysis can estimate traction force from bead displacement. However, most algorithms estimate substrate stresses independently of cell boundary, which results in poor estimation accuracy in low-density bead environments. To achieve accurate force estimation at low density, we proposed a Bayesian traction force estimation (BTFE) algorithm that incorporates cell-boundary-dependent force as a prior. We evaluated the performance of the proposed algorithm using synthetic data generated with mathematical models of cells and TFM substrates. BTFE outperformed other methods, especially in low-density bead conditions. In addition, the BTFE algorithm provided a reasonable force estimation using TFM images from the experiment., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2023 Biophysical Society. Published by Elsevier Inc. All rights reserved.)