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Ti alloys have attracted continuing research attention as promising biomaterials due to their superior corrosion resistance and biocompatibility and excellent mechanical properties. Metastable β-type Ti alloys also provide several unique properties such as low Young’s modulus, shape memory effect, and superelasticity. Such unique properties are predominantly attributed to the phase stability and reversible martensitic transformation. In this study, the effects of the Nb and Zr contents on phase constitution, transformation temperature, deformation behavior, and Young’s modulus were investigated. Ti–Nb and Ti–Nb–Zr alloys over a wide composition range, i.e., Ti–(18–40)Nb, Ti–(15–40)Nb–4Zr, Ti–(16–40)Nb–8Zr, Ti–(15–40)Nb–12Zr, Ti–(12–17)Nb–18Zr, were fabricated and their properties were characterized. The phase boundary between the β phase and the α′′ martensite phase was clarified. The lower limit content of Nb to suppress the martensitic transformation and to obtain a single β phase at room temperature decreased with increasing Zr content. The Ti–25Nb, Ti–22Nb–4Zr, Ti–19Nb–8Zr, Ti–17Nb–12Zr and Ti–14Nb–18Zr alloys exhibit the lowest Young’s modulus among Ti–Nb–Zr alloys with Zr content of 0, 4, 8, 12, and 18 at.%, respectively. Particularly, the Ti–14Nb–18Zr alloy exhibits a very low Young’s modulus less than 40 GPa. Correlation among alloy composition, phase stability, and Young’s modulus was discussed.

Hearing loss (HL) affects more than 1.5 billion people worldwide and remains a leading cause of disability across the lifespan. While genetic predispositions, otitis media (OM), and cholesteatoma are well-recognized contributors, Eustachian tube dysfunction (ETD) is an underappreciated but pivotal determinant of auditory morbidity. By impairing middle ear pressure (MEP) regulation, ETD drives conductive hearing loss (CHL) through stiffness and mass-loading effects, contributes to sensorineural hearing loss (SNHL) via altered window mechanics and vascular stress, and produces mixed hearing loss (MHL) when these pathways converge. A characteristic clinical trajectory emerges in which conductive deficits often resolve quickly with restored ventilation, whereas sensorineural impairment requires prolonged, physiology-restoring intervention, resulting in transient or persistent MHL. This review integrates mechanistic insights with clinical manifestations, diagnostic approaches, and therapeutic options. Diagnostic frameworks that combine patient-reported outcomes with objective biomarkers such as wideband absorbance, tympanometry, and advanced imaging enable reproducible identification of ETD-related morbidity. Conventional treatments, including tympanostomy tubes and balloon dilation, offer short-term benefit but rarely normalize tubal physiology. In contrast, Eustachian tube catheterization (ETC) has emerged as a promising, mechanism-based intervention capable of reestablishing dynamic tubal opening and MEP regulation. Looking forward, integration of physiology-based frameworks with personalized diagnostics and advanced tools such as artificial intelligence (AI) may help prevent progression from reversible conductive deficits to irreversible SNHL or MHL.

Railway point devices act as actuators that provide different routes to trains by driving switchblades from the current position to the opposite one. Point failure can significantly affect railway operations, with potentially disastrous consequences. Therefore, early detection of anomalies is critical for monitoring and managing the condition of rail infrastructure. We present a data mining solution that utilizes audio data to efficiently detect and diagnose faults in railway condition monitoring systems. The system enables extracting mel-frequency cepstrum coefficients (MFCCs) from audio data with reduced feature dimensions using attribute subset selection, and employs support vector machines (SVMs) for early detection and classification of anomalies. Experimental results show that the system enables cost-effective detection and diagnosis of faults using a cheap microphone, with accuracy exceeding 94.1% whether used alone or in combination with other known methods.

Lateral cephalograms and related analysis constitute representative methods for orthodontic treatment. However, since conventional cephalometric radiographs display a three-dimensional structure on a two-dimensional plane, inaccuracies may be produced when quantitative evaluation is required. Cone-beam computed tomography (CBCT) has minimal image distortion, and important parts can be observed without overlapping. It provides a high-resolution three-dimensional image at a relatively low dose and cost, but still shows a higher dose than a lateral cephalogram. It is especially true for children who are more susceptible to radiation doses and often have difficult diagnoses. A conventional lateral cephalometric radiograph can be obtained by reconstructing the Digital Imaging and Communications in Medicine data obtained from CBCT. This study evaluated the applicability and consistency of lateral cephalograms generated by CBCT using an artificial intelligence analysis program. Group I comprised conventional lateral cephalometric radiographs, group II comprised lateral cephalometric radiographs generated from CBCT using OnDemand 3D, and group III comprised lateral cephalometric radiographs generated from CBCT using Invivo5. All measurements in the three groups showed non-significant results. Therefore, a CBCT scan and artificial intelligence programs are efficient means when performing orthodontic analysis on pediatric or orthodontic patients for orthodontic diagnosis and planning.

The immune system has traditionally been divided into innate and adaptive branches, with immunological memory considered a hallmark of adaptive immunity. However, recent studies reveal that innate immune cells can also exhibit memory-like properties, known as trained immunity. This phenomenon involves the long-term functional reprogramming of innate immune cells following exposure to exogenous or endogenous stimuli, mediated by epigenetic and metabolic changes. Trained immunity enhances responses to subsequent unrelated challenges and serves as a protective mechanism against reinfection. Nonetheless, it may also contribute to the development of chronic inflammatory diseases such as autoimmune disorders, allergies and atherosclerosis. Whereas much of the research has focused on pathogen-associated molecular patterns as inducers of trained immunity, emerging evidence highlights that sterile inflammation, driven by damage-associated molecular patterns and lifestyle-associated molecular patterns, can similarly induce this immune adaptation. Here we examine the molecular mechanisms underlying damage-associated molecular pattern- and lifestyle-associated molecular pattern-induced trained immunity and their roles in chronic inflammation. This Review also discusses central trained immunity, characterized by the durable reprogramming of hematopoietic stem and progenitor cells, and its implications in disease progression. Finally, potential therapeutic strategies targeting metabolic and epigenetic pathways are considered. Understanding noninfectious stimuli-induced trained immunity offers new insights into chronic inflammatory disease management. trained immunity reveals innate cells can remember challenges The immune system has two parts: innate and adaptive immunity. Scientists used to think only adaptive immunity had memory, but recent studies show innate immunity can also remember. Trained immunity involves long-term changes in innate immune cells, such as macrophages, due to vaccines or other stimuli, leading to better responses to future infections. Researchers have found that not just infections but also noninfectious factors such as diet and stress can trigger trained immunity. This Review reviews recent findings on how certain molecules, called damage-associated molecular patterns and lifestyle-associated molecular patterns, can induce trained immunity. These molecules are released from damaged cells or accumulated owing to poor clearance and can cause chronic inflammation, contributing to diseases such as atherosclerosis and chronic kidney disease. The Review concludes that understanding trained immunity could lead to new treatments for chronic inflammatory diseases by targeting these pathways. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.

Traditionally, Thunb. (GJ) extract has been used to treat headaches and dizziness. We hypothesize that GJ exhibits anti-platelet activity that may prevent ischemic events to alleviate these symptoms. In this study, we investigated the anti-platelet activity of GJ as a potential mechanism for enhancing blood flow and preventing vessel occlusion. Platelets were stimulated with collagen, adenosine diphosphate (ADP) or thrombin. Platelet aggregation was carried out using a platelet aggregometer with washed platelets from Sprague-Dawley rats. We observed the mobilization of calcium ions using Fura-2AM and adenosine triphosphate (ATP) release via a luminometer. The activation of integrin αIIbβ3 and population of platelet-neutrophil aggregates (PNAs) were investigated using flow cytometry. Platelet shape change was observed using scanning electron microscopy and transmission electron microscopy. GJ extract inhibited collagen, ADP and thrombin-induced platelet aggregation. It effectively prevented the mobilization of calcium ions, ATP secretion, and serotonin release while thromboxane B2 levels did not change. Moreover, GJ inhibited the inside-out and outside-in signaling of integrin αIIbβ3. Notably, GJ treatment led to elevated expression of cyclic guanine monophosphate (GMP) (but not cyclic adenosine monophosphate). The protein expressions in the PI3K/Akt pathway were inhibited and platelet shape change was prevented. Finally, GJ treatment resulted in a decreased population of PNAs . GJ exhibits potent anti-platelet activity acting by upregulating cGMP. It holds promise as a potential candidate for supplementation in patients with cardiovascular disease and thrombosis.

Background: Chronic pain and cancer interact bidirectionally, with pain enhancing sensory peptides and potentially promoting tumor growth. Despite this, most chemotherapy-induced neuropathic pain (CIPN) studies overlook the contribution of cancer itself to neuropathy, focusing instead on chemotherapy-induced mechanisms. Animal models of chemotherapy-induced neuropathic pain (CINP) have been developed by injecting chemotherapeutic drugs such as paclitaxel into normal animals without cancer. This study aimed to develop a new model in mouse mammary tumor virus–polyomavirus middle T antigen (MMTV-PyMT) mice, a widely used breast cancer model with normal immune function. Results: The percentage of positive response (PPR) of paclitaxel-injected MMTV-PyMT mice increased (about 20%; baseline, 10%) on day 4, reached the highest levels (50%–60%) on days 6–9, and then plateaued by day 29. In comparison, the PPR of paclitaxel-injected C57BL/6 was less than 10% on days 0–6, was about 40% on day 9, and then plateaued by day 29. Breast tumor–bearing mice exhibited an earlier onset and greater severity of paclitaxel-induced pain behaviors than tumor-free C57BL/6 mice. Systemic LGK-974 ameliorated paclitaxel-induced pain behaviors in MMTV-PyMT mice. Active β-catenin was detected in neurons and satellite cells of the dorsal root ganglia. Conclusions: Paclitaxel-induced neuropathic pain model in breast tumor–bearing female MMTV-PyMT mice may be a useful animal model for investigating the analgesic effects and underlying mechanisms for CINP in breast cancer patients as well as the interplay between CINP development and cancer progression.

Branched-chain amino acids (BCAAs), particularly leucine, are indispensable AAs for immune regulation through metabolic rewiring. However, the molecular mechanism underlying this phenomenon remains unclear. Our investigation revealed that T-cell receptor (TCR)-activated human CD4 + T cells increase the expression of BCAT1, a cytosolic enzyme responsible for BCAA catabolism, and SLC7A5, a major BCAA transporter. This upregulation facilitates increased leucine influx and catabolism, which are particularly crucial for Th17 responses. Activated CD4 + T cells induce an alternative pathway of cytosolic leucine catabolism, generating a pivotal metabolite, β-hydroxy β-methylbutyric acid (HMB), by acting on BCAT1 and 4-hydroxyphenylpyruvate dioxygenase (HPD)/HPD-like protein (HPDL). Inhibition of BCAT1-mediated cytosolic leucine metabolism, either with BCAT1 inhibitor 2 (Bi2) or through BCAT1, HPD, or HPDL silencing using shRNA, attenuates IL-17 production, whereas HMB supplementation abrogates this effect. Mechanistically, HMB contributes to the regulation of the mTORC1-HIF1α pathway, a major signaling pathway for IL-17 production, by increasing the mRNA expression of HIF1α. This finding was corroborated by the observation that treatment with L-β-homoleucine (LβhL), a leucine analog and competitive inhibitor of BCAT1, decreased IL-17 production by TCR-activated CD4 + T cells. In an in vivo experimental autoimmune encephalomyelitis (EAE) model, blockade of BCAT1-mediated leucine catabolism, either through a BCAT1 inhibitor or LβhL treatment, mitigated EAE severity by decreasing HIF1α expression and IL-17 production in spinal cord mononuclear cells. Our findings elucidate the role of BCAT1-mediated cytoplasmic leucine catabolism in modulating IL-17 production via HMB-mediated regulation of mTORC1-HIF1α, providing insights into its relevance to inflammatory conditions. Immune regulation: leucine’s role in Th17 response modulation T-cell, a type of infection-fighting white blood cell, alter their metabolic process, relying heavily on amino acids, the building blocks of proteins. This study investigates how T cells use the amino acid leucine to power their response. Researchers conducted experiments with human T-cell and a mouse model of autoimmune disease, a condition where the body attacks its own cells. They studied how leucine’s metabolic process affects T-cell function. The study discovered that a specific process involving leucine’s metabolic pathway in T cells is vital for their ability to produce IL-17. Blocking a crucial enzyme reduced IL-17 production and eased symptoms in a mouse model of autoimmune disease. These findings underline the importance of leucine’s metabolic process in T-cell function and suggest a potential target for treating autoimmune diseases more effectively, offering hope for new treatments. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.