Explore the vast range of titles available.

East and Southeast Asia (ESEA) are facing age-related eye health issues. Low-vision rehabilitation (LVR), which is a special rehabilitation service for individuals with vision impairment, is a promising solution for these health issues; however, poor accessibility to LVR services has been reported globally, including ESEA. Therefore, this scoping review aimed to summarize and understand the barriers to accessing LVR services in ESEA. In total, 20 articles were ultimately considered eligible for this scoping review after an electronic database search using MEDLINE (PubMed), Web of Science, Academic Search Ultimate (EBSCO), and Ichushi-Web (Japanese medical literature database), and an independent review by two reviewers. Twenty-one potential barrier factors were identified in the full-text review. Notably, age, education, economic status, “previous experience using eye care service”, and “knowledge, information, and awareness” were the possible barrier factors that were examined for their association with LVR utilization, with supportive evidence in many eligible studies. We also identified research gaps relating to geographical and ethnic diversity, the scope of LVR services, and barriers among eligible articles. Therefore, by conducting further studies addressing the research gaps identified in this scoping review, these findings can be used to make LVR services more accessible to people in ESEA.

Many mouse models of Alzheimer's disease (AD) rely on overexpression of amyloid precursor (APP) transgenes, which makes it difficult to tease out which effects are truly disease-relevant and which are induced by the overexpression. In this study, the authors describe several new knock-in AD model mice that express mutant APP at near physiological levels. Experimental studies of Alzheimer's disease have largely depended on transgenic mice overexpressing amyloid precursor protein (APP). These mice, however, suffer from artificial phenotypes because, in addition to amyloid β peptide (Aβ), they overproduce other APP fragments. We generated knock-in mice that harbor Swedish and Beyreuther/Iberian mutations with and without the Arctic mutation in the APP gene. The mice showed typical Aβ pathology, neuroinflammation and memory impairment in an age-dependent manner.

This study aimed to evaluate the in vitro effect of the novel bioactive adhesive monomer CMET, a calcium salt of 4-methacryloxyethyl trimellitate acid (4-MET), on human dental pulp stem cells (hDPSCs) and its capacity to induce tertiary dentin formation in a rat pulp injury model. Aqueous solutions of four tested materials [4-MET, CMET, Ca(OH)2, and mineral trioxide aggregate (MTA)] were added to the culture medium upon confluence, and solvent (dH2O) was used as a control. Cell proliferation was assessed using the Cell Counting Kit-8 assay, and cell differentiation was evaluated by real-time quantitative reverse transcription-polymerase chain reaction. The mineralization-inducing capacity was evaluated using alizarin red S staining and an alkaline phosphatase activity assay. For an in vivo experiment, a mechanical pulp exposure model was prepared on Wistar rats; damaged pulp was capped with Ca(OH)2 or CMET. Cavities were sealed with composite resin, and specimens were assessed after 14 and 28 days. The in vitro results showed that CMET exhibited the lowest cytotoxicity and highest odontogenic differentiation capacity among all tested materials. The favorable outcome on cell mineralization after treatment with CMET involved p38 and c-Jun N-terminal kinases signaling. The nuclear factor kappa B pathway was involved in the CMET-induced mRNA expression of odontogenic markers. Similar to Ca(OH)2, CMET produced a continuous hard tissue bridge at the pulp exposure site, but treatment with only CMET produced a regular dentinal tubule pattern. The findings suggest that (1) the evaluated novel bioactive adhesive monomer provides favorable biocompatibility and odontogenic induction capacity and that (2) CMET might be a very promising adjunctive for pulp-capping materials.

Alzheimer’s disease (AD) is associated with progressive neuronal degeneration as amyloid-beta (Aβ) and tau proteins accumulate in the brain. Glial cells were recently reported to play an important role in the development of AD. However, little is known about the role of oligodendrocytes in AD pathogenesis. Here, we describe a disease-associated subpopulation of oligodendrocytes that is present during progression of AD-like pathology in the male App NL-G-F and male 5xFAD AD mouse brains and in postmortem AD human brains using single-cell RNA sequencing analysis. Aberrant Erk1/2 signaling was found to be associated with the activation of disease-associated oligodendrocytes (DAOs) in male App NL-G-F mouse brains. Notably, inhibition of Erk1/2 signaling in DAOs rescued impaired axonal myelination and ameliorated Aβ-associated pathologies and cognitive decline in the male App NL-G-F AD mouse model. Oligodendrocytes have been increasingly shown to be involved in Alzheimer’s disease (AD). Here, the authors perform single-cell RNA-sequencing on APP NL-G-F mice and describe a disease-associated oligodendrocyte (DAO) population. They find inhibition of Erk1/2 signaling in DAOs rescues impaired axonal myelination and cognitive decline in an AD mouse model.

Sca l eS is a tissue clearing method for light and electron microscopy featuring stable tissue preservation for immunochemical and genetic labeling of tissue for 3D signal rendering. The technique enables quantitative and reproducible reconstructions of aged and diseased tissue in animal models and patients for high resolution optical pathology. Optical clearing methods facilitate deep biological imaging by mitigating light scattering in situ . Multi-scale high-resolution imaging requires preservation of tissue integrity for accurate signal reconstruction. However, existing clearing reagents contain chemical components that could compromise tissue structure, preventing reproducible anatomical and fluorescence signal stability. We developed Sca l eS, a sorbitol-based optical clearing method that provides stable tissue preservation for immunochemical labeling and three-dimensional (3D) signal rendering. Sca l eS permitted optical reconstructions of aged and diseased brain in Alzheimer's disease models, including mapping of 3D networks of amyloid plaques, neurons and microglia, and multi-scale tracking of single plaques by successive fluorescence and electron microscopy. Human clinical samples from Alzheimer's disease patients analyzed via reversible optical re-sectioning illuminated plaque pathogenesis in the z axis. Comparative benchmarking of contemporary clearing agents showed superior signal and structure preservation by Sca l eS. These findings suggest that Sca l eS is a simple and reproducible method for accurate visualization of biological tissue.

Type I collagen (COL-1) is the prevailing component of the extracellular matrix in a number of tissues including skin, ligament, cartilage, bone, and dentin. It is the most widely used tissue-derived natural polymer. Currently, mammalian animals, including pig, cow, and rat, are the three major sources for purification of COL-1. To reduce the risk of zoonotic infectious diseases transmission, minimize the possibility of immunogenic reaction, and avoid problems related to religious issues, exploration of new sources (other than mammalian animals) for the purification of type I collagen is highly desirable. Hence, the purpose of the current study was to investigate the in vitro responses of MDPC-23 to type I collagen isolated from tilapia scale in terms of cellular proliferation, differentiation, and mineralization. The results suggested that tilapia scale collagen exhibited comparable biocompatibility to porcine skin collagen, indicating it might be a potential alternative to type I collagen from mammals in the application for tissue regeneration in oral-maxillofacial area.

Hydrogen transport in solids, applied in electrochemical devices such as fuel cells and electrolysis cells, is key to sustainable energy societies. Although using proton (H + ) conductors is an attractive choice, practical conductivity at intermediate temperatures (200–400 °C), which would be ideal for most energy and chemical conversion applications, remains a challenge. Alternatively, hydride ions (H – ), that is, monovalent anions with high polarizability, can be considered a promising charge carrier that facilitates fast ionic conduction in solids. Here, we report a K 2 NiF 4 -type Ba–Li oxyhydride with an appreciable amount of hydrogen vacancies that presents long-range order at room temperature. Increasing the temperature results in the disappearance of the vacancy ordering, triggering a high and essentially temperature-independent H – conductivity of more than 0.01 S cm –1 above 315 °C. Such a remarkable H – conducting nature at intermediate temperatures is anticipated to be important for energy and chemical conversion devices. Although using proton (H + ) conductors is attractive for energy applications, practical conductivity at intermediate temperatures (200–400 °C) remains a challenge. A K 2 NiF 4 -type Ba–Li oxyhydride is shown to exhibit a temperature-independent hydrogen conductivity of more than 0.01 S cm –1 above 315 °C.

Metabolic dysfunction‐associated steatotic liver disease (MASLD) is characterized by intense deposition of fat globules in the hepatic parenchyma that could potentially progress to liver cirrhosis and hepatocellular carcinoma. Here, we evaluated a rat model to study the molecular pathogenesis of the spectrum of MASLD and to screen therapeutic agents. SHRSP5/Dmcr rats were fed a high‐fat and cholesterol (HFC) diet for a period of 12 weeks and evaluated for the development of steatosis (MASLD), steatohepatitis, fibrosis and cirrhosis. A group of animals were sacrificed at the end of the 4th, 6th, 8th and 12th weeks from the beginning of the experiment, along with the control rats that received normal diet. Blood and liver samples were collected for biochemical and histopathological evaluations. Immunohistochemical staining was performed for α‐SMA and Collagen Type I. Histopathological examinations demonstrated steatosis at the 4th week, steatohepatitis with progressive fibrosis at the 6th week, advanced fibrosis with bridging at the 8th week and cirrhosis at the 12th week. Biochemical markers and staining for α‐SMA and Collagen Type I demonstrated the progression of steatosis to steatohepatitis, hepatic fibrosis and liver cirrhosis in a stepwise manner. Control animals fed a normal diet did not show any biochemical or histopathological alterations. The results of the present study clearly demonstrated that the HFC diet‐induced model of steatosis, steatohepatitis, hepatic fibrosis and cirrhosis is a feasible, quick and appropriate animal model to study the molecular pathogenesis of the spectrum of MASLD and to screen potent therapeutic agents.

Background Recent studies suggest that microglia contribute to tau pathology progression in Alzheimer’s disease. Amyloid plaque accumulation transforms microglia, the primary innate immune cells in the brain, into neurodegenerative microglia (MGnD), which exhibit enhanced phagocytosis of plaques, apoptotic neurons and dystrophic neurites containing aggregated and phosphorylated tau (p-tau). It remains unclear how microglia promote disease progression while actively phagocytosing pathological proteins, therefore ameliorating pathology. Methods Adeno-associated virus expressing P301L tau mutant (AAV-P301L-tau) was stereotaxically injected into the medial entorhinal cortex (MEC) in C57BL/6 (WT) and humanized APP mutant knock-in homozygote ( App NL-G-F ) mice at 5 months of age. Mice were fed either chow containing a colony stimulating factor-1 receptor inhibitor (PLX5622) or control chow from 4 to 6 months of age to test the effect of microglia depletion. Animals were tested at 6 months of age for immunofluorescence, biochemistry, and FACS of microglia. In order to monitor microglial extracellular vesicle secretion in vivo, a novel lentiviral EV reporter system was engineered to express mEmerald-CD9 (mE-CD9) specifically in microglia, which was injected into the same region of MEC. Results Expressing P301L tau mutant in the MEC induced tau propagation to the granule cell layer of the hippocampal dentate gyrus, which was significantly exacerbated in App NL-G-F mice compared to WT control mice. Administration of PLX5622 depleted nearly all microglia in mouse brains and dramatically reduced propagation of p-tau in WT and to a greater extent in App NL-G-F mice, although it increased plaque burden and plaque-associated p-tau + dystrophic neurites. Plaque-associated MGnD microglia strongly expressed an EV marker, tumor susceptibility gene 101, indicative of heightened synthesis of EVs. Intracortical injection of mE-CD9 lentivirus successfully induced microglia-specific expression of mE-CD9 + EV particles, which were significantly enhanced in Mac2 + MGnD microglia compared to Mac2 − homeostatic microglia. Finally, consecutive intracortical injection of mE-CD9 lentivirus and AAV-P301L-tau into App NL-G-F mice revealed encapsulation of p-tau in microglia-specific mE-CD9 + EVs as determined by super-resolution microscopy and immuno-electron microscopy. Discussion Our findings suggest that MGnD microglia hyper-secrete p-tau + EVs while compacting Aβ plaques and clearing NP tau, which we propose as a novel mechanistic link between amyloid plaque deposition and exacerbation of tau propagation in App NL-G-F mice.

Producing a single crystal is expensive because of low mass productivity. Therefore, many metallic materials are being used in polycrystalline form, even though material properties are superior in a single crystal. Here we show that an extraordinarily large Cu-Al-Mn single crystal can be obtained by abnormal grain growth (AGG) induced by simple heat treatment with high mass productivity. In AGG, the sub-boundary energy introduced by cyclic heat treatment (CHT) is dominant in the driving pressure, and the grain boundary migration rate is accelerated by repeating the low-temperature CHT due to the increase of the sub-boundary energy. With such treatment, fabrication of single crystal bars 70 cm in length is achieved. This result ensures that the range of applications of shape memory alloys will spread beyond small-sized devices to large-scale components and may enable new applications of single crystals in other metallic and ceramics materials having similar microstructural features. Growing large single crystals cheaply and reliably for structural applications remains challenging. Here, the authors combine accelerated abnormal grain growth and cyclic heat treatments to grow a superelastic shape memory alloy single crystal to 70 cm.