Search Results (8,407)

Background: Hepatopancreatobiliary (HPB) surgery is among the most complex domains in oncologic care, where decisions entail significant risk–benefit considerations. Artificial intelligence (AI) has emerged as a promising tool for improving individualized decision-making through enhanced risk stratification, complication prediction, and survival modeling. However, its role in HPB oncologic surgery has not been comprehensively assessed. Methods: This systematic review was conducted in accordance with PRISMA guidelines and registered with PROSPERO ID: CRD420251114173. A comprehensive search across six databases was performed through 30 May 2025. Eligible studies evaluated AI applications in risk–benefit assessment in HPB cancer surgery. Inclusion criteria encompassed peer-reviewed, English-language studies involving human s ubjects. Two independent reviewers conducted study selection, data extraction, and quality appraisal. Results: Thirteen studies published between 2020 and 2024 met the inclusion criteria. Most studies employed retrospective designs with sample sizes ranging from small institutional cohorts to large national databases. AI models were developed for cancer risk prediction (n = 9), postoperative complication modeling (n = 4), and survival prediction (n = 3). Common algorithms included Random Forest, XGBoost, Decision Trees, Artificial Neural Networks, and Transformer-based models. While internal performance metrics were generally favorable, external validation was reported in only five studies, and calibration metrics were often lacking. Integration into clinical workflows was described in just two studies. No study addressed cost-effectiveness or patient perspectives. Overall risk of bias was moderate to high, primarily due to retrospective designs and incomplete reporting. Conclusions: AI demonstrates early promise in augmenting risk–benefit assessment for HPB oncologic surgery, particularly in predictive modeling. However, its clinical utility remains limited by methodological weaknesses and a lack of real-world integration. Future research should focus on prospective, multicenter validation, standardized reporting, clinical implementation, cost-effectiveness analysis, and the incorporation of patient-centered outcomes. Full article

To address the challenges of short dwell time near top dead center (TDC) and uneven heat release, this paper presents a comprehensive analysis of the effects of different ignition schemes on combustion characteristics, flame formation and development, and emissions. A three-dimensional model of coupled reaction’s kinetic mechanism was established using Converge 3.0 and validated by experimental data. The results show that ignition position, whether synchronous or asynchronous changes, significantly influence pressure. The pressure in synchronous cases can reach up to 62.5 bar, representing a 10.8% increase, exhibiting a distinct upward trend with advanced ignition position. In asynchronous cases, the pressure variation shows a distinct nonlinear characteristic due to the negative effects of in-cylinder airflow and flame core collision. When the ignition position is advanced, the ignition delay increases for both synchronous and asynchronous strategies. However, for synchronous cases, the combustion duration is reduced by up to 1.5 ms, whereas for asynchronous cases, the reduction is only 0.135 ms. Regardless of the schemes, the layout and the strong counterclockwise swirl lead to the flame core gradually developing from right to left, ultimately engulfing the left-side flame core. Compared then to that case, the left and right flame kernels may collide prematurely, leading to incomplete local combustion and consequently reducing combustion efficiency. Compared to synchronous changes, the emission differences during asynchronous changes are smaller and maintained at a relatively low level. Full article

To solve the problems of large root damage and incomplete seedling blocks (SBs) in rice machine transplanting, this study numerically optimized the root blanket-cutting device for rice blanket seedling cutting and throwing transplanters based on the discrete element method (DEM) and multi-body dynamics (MBD) coupling method. A longitudinal sliding cutter (LSC)–substrate–root interaction model was established. Based on the simulation tests of Center Composite Design and response surface analysis, the sliding angle and cutter shaft speed of the LSCs arranged at the circumferential angles (CAs) of 0°, 30°, and 60° were optimized. The simulation results indicated that the LSC arrangement CA significantly affected the cutting performance, with the optimal configuration achieved at a CA of 60°. Under the optimal parameters (sliding angle of 57°, cutter shaft speed of 65.3 r/min), the average deviation between the simulated and physical tests was less than 11%, and the reliability of the parameters was verified. A seedling needle–substrate–root interaction model was established. The Box–Behnken Design method was applied to conduct simulation tests and response surface optimization, focusing on the picking angle, needle width, and rotary gearbox speed. The simulation results showed that the picking angle was the key influencing factor. Under the optimal parameters (picking angle of 20°, seedling needle width of 15 mm, rotary gearbox speed of 209 r/min), the average deviation between the simulated and physical tests was less than 10%, which met the design requirements. This study provides a new solution for reducing root injury, improving SB integrity, and reducing energy consumption in rice transplanting, and provides theoretical and technical references for optimizing transplanting machinery structure and selecting working parameters. Full article

Based on the problem of incomplete mining of Additive Manufacturing (AM) potential caused by the limitations of current Design for Additive Manufacturing (DFAM) methods, this paper proposes to integrate Additive Manufacturing and axiomatic design to obtain the global conceptual design method of products to be manufactured with AM. In response to the lower process dependence of AM technology compared to traditional processes, two integration measures of “influence region division” and “process domain forward” are proposed, and finally, the axiomatic design process for AM is obtained. Taking the assembly-free integrated design of mechanical fingers imitating dexterous hands as an example, the conceptual design method studied was validated. The application of innovative features such as flexible finger joints and lattice-filled finger joints shows that the design method proposed in this paper can deeply tap into the manufacturing potential of AM, achieve lightweight and integrated molding of products, which provides useful references for designers. Full article

Nutritional factors play a crucial role in many gynecological disorders, particularly those influenced by estrogen. Uterine fibroids are benign tumors that affect a large proportion of women of reproductive age, especially between 30 and 40 years. These lesions may cause significant symptoms, including pelvic pain, heavy menstrual bleeding, and infertility. In younger women, the onset of fibroids is often associated with familial and genetic predisposition, whereas in adulthood, hormonal influences linked to environmental factors and states of exogenous or endogenous hyperestrogenism are more frequently observed. In both contexts, supportive management through an appropriate diet may provide clinical benefit. Although the precise pathogenesis remains incompletely understood, hormonal, genetic, and environmental components—particularly hyperestrogenism—are considered key contributors to fibroid development. Current evidence suggests that consumption of saturated fats, particularly from red meat and full-fat dairy, may raise circulating estrogen concentrations and contribute to the development of fibroids. In contrast, diets abundant in fiber, fruits, and vegetables appear to exert a protective effect, potentially lowering fibroid risk. Obesity, through increased aromatization and consequent estrogen production, also represents an established risk factor. This narrative review aims to explore the role of nutritional determinants in the onset and progression of uterine fibroids, with a specific focus on the impact of individual nutrients, foods, and dietary patterns on clinical outcomes. Particular emphasis is placed on obesity and macronutrient composition (e.g., high-fat versus high-fiber dietary regimens) as potential modulators of circulating estrogen levels and, consequently, fibroid growth dynamics. Furthermore, the potential of nutritional strategies as complementary therapeutic approaches, capable of integrating established clinical practices, is examined. Full article

Autoimmune gastritis (AIG) is a chronic, organ-specific autoimmune disease characterized by progressive destruction of gastric parietal cells driven by autoreactive CD4⁺ T-cells, epithelial stress pathways, and microbial factors. Parietal cell loss results in achlorhydria, intrinsic factor deficiency, and vitamin B12 malabsorption, ultimately leading to pernicious anemia. Compensatory hypergastrinemia promotes enterochromaffin-like (ECL) cell hyperplasia and contributes to the development of type 1 gastric neuroendocrine neoplasms (gNENs). These clinical consequences are well recognized, yet the cellular and molecular mechanisms driving mucosal atrophy and neoplastic transformation remain incompletely defined. Recent advances highlight the role of endoplasmic reticulum stress, impaired autophagy, innate immune effectors, and dysbiosis in perpetuating inflammation and epithelial injury. The frequent coexistence of AIG with other autoimmune disorders further adds to its clinical complexity. Therapeutic options remain limited, spanning vitamin B12 replacement and endoscopic management to emerging targeted approaches. Netazepide, a gastrin/CCK2 receptor antagonist, is the only agent tested in clinical trials, whereas interventions targeting ER stress, autophagy, immune tolerance, or microbiome composition are still in the preclinical stage. Clarifying these mechanisms is crucial to improve biomarker development, optimize surveillance, and identify targeted therapies to prevent neoplastic transformation. Full article

Congenital hearing loss, frequently resulting from defective hair cells, remains poorly understood due to the incomplete identification of key pathogenic genes. Oncomodulin (OCM) is a kind of calcium-binding protein (CaBP) that regulates diverse cellular processes and is thought to play crucial roles in auditory function. In teleost fish, parvalbumin 8 (pvalb8) and parvalbumin 9 (pvalb9) belong to the oncomodulin lineage and are highly expressed in hair cells. In this study, we first reported the oncomodulin lineage function in fish and identified pvalb8 as an essential regulator of hair cell development. Single-cell RNA sequencing (scRNA-seq) and whole-mount in situ hybridization (WISH) revealed that pvalb8 is highly and specifically expressed in supporting cells and hair cells. Functional loss of pvalb8, achieved via CRISPR/Cas9 knockout or morpholino knockdown, resulted in reduced neuromast size and a significant decrease in neuromast hair cell number, leading to auditory behavioral deficits. In addition, pvalb9 mutants exhibited hair cell defects similar to those observed in pvalb8 mutants, including a significant reduction in hair cell number. Moreover, pvalb8 loss strongly inhibited the proliferation of supporting cells, which likely accounts for the reduced number of differentiated hair cells. The expression levels of Wnt target genes, axin2, ccnd1, and myca, were all significantly reduced in pvalb8 mutants compared to control zebrafish, while activation of the Wnt signaling pathway rescued the hair cell loss observed in pvalb8 mutants, indicating that pvalb8 promotes hair cell development via Wnt-dependent proliferative signaling. These findings highlight pvalb8 as a critical factor in the regulation of auditory hair cell formation and function in zebrafish, offering new insights into the role of oncomodulin lineage in sensory cell development. Full article

To address the issue of hysteresis nonlinearity adversely affecting the tracking accuracy of piezoelectric actuators, an improved particle swarm optimization (PSO) algorithm is proposed to improve the accuracy of hysteresis model parameter identification. Additionally, a discrete-time linear quadratic optimal tracking (DLQT) control strategy incorporating hysteresis compensation is developed to improve tracking performance. This study employs the Hammerstein model to characterize the nonlinear hysteresis behavior of piezoelectric actuators. Regarding parameter identification, the conventional PSO algorithm tends to suffer from premature convergence and being trapped in local optima. To address this, a cross-variation mechanism is introduced to enhance population diversity and improve global search ability. Furthermore, adaptive and dynamically adjustable inertia weights are designed based on evolutionary factors to balance exploration and exploitation, thereby enhancing convergence and identification accuracy. The inertia weights and learning factors are adaptively adjusted based on the evolutionary factor to balance local and global search capabilities and accelerate convergence. Benchmark function tests and model identification experiments demonstrate the improved algorithm’s superior convergence speed and accuracy. In terms of control strategy, a hysteresis compensator based on an asymmetric hysteresis model is designed to improve system linearity. To address the issues of incomplete hysteresis compensation and low tracking accuracy, a DLQT controller is developed based on hysteresis compensation. Hardware-in-the-loop tracking control experiments using single and composite frequency reference signals show that the relative error is below 3.3% in the no-load case and below 4.5% in the loaded case. Compared with the baseline method, the proposed control strategy achieves lower root-mean-square error and maximum steady-state error, demonstrating its effectiveness. Full article

Immune checkpoint inhibitors (ICIs), including PD-L1 inhibitors, have been approved by the FDA for the treatment of cancers; however, only a small number of cancer patients benefit from these ICIs. Furthermore, the development of drug resistance to this type of treatment is often inevitable. The mechanisms of resistance to PD-L1 inhibitors can be attributed, in part, to an incomplete understanding of the regulation of PD-L1 protein expression. In this study, we identified the role of the E3 ligase GP78, also known as the Autocrine Motility Factor Receptor (AMFR), in the regulation of PD-L1 protein levels. We show that GP78 physically interacts with PD-L1, which is confirmed by IP and Western blotting and is supported by molecular modelling using AlphaFold2. Our modeling studies predict that the interface amino acids of the Ig1 domain of PD-L1 interact with the RING domain and a β-hairpin preceding the CUE domain of GP78. The crystal structure of the PD-1/PD-L1 complex reveals that the interaction with PD-1 is mediated by the Ig1 domain of PD-L1. Furthermore, proteasomal degradation of PD-L1 has been observed via GP78-mediated K48-linked ubiquitination, indicating a key regulatory role for GP78 in the downregulation of PD-L1. Because GP78 expression is inversely correlated with PD-L1 levels in cancer, these findings may have clinical implications for predicting tumor immune evasion and patient response to PD-1/PD-L1 blockade therapies. Taken together, these findings identify a previously unknown mechanism by which GP78 targets PD-L1 for ubiquitination and subsequent degradation in cancer cells, and suggest that blocking the interaction between PD-L1 and PD-1 by an E3 ligase is a novel strategy to improve immunotherapies for cancer patients. Full article

Schizophrenia is a prevailing yet severely debilitating psychiatric disorder characterized by a convoluted etiology. Although antipsychotics have been available for over half a century, they primarily mitigate symptoms rather than providing definitive care. This limitation suggests that the neurotransmitter systems targeted by these medications are not the root cause of the disorder. Ongoing research seeks to elucidate the cellular, molecular, and circuitry pathways that contribute to the development of schizophrenia. Unfortunately, its precise pathogenesis remains incompletely understood. Accumulating evidence implicates dysregulated neurogenesis and aberrant neurodevelopmental processes as key contributors to disease progression. Recent advances in proteomics and imaging technology have facilitated the emergence of novel models of schizophrenia, emphasizing the roles of neuroinflammation, sex steroids, and cortisol. This paper aims to organize and map the intercorrelations and potential causal effects between various mechanistic models to gain deeper insight on how these mechanisms contribute to the cause, risks, and symptoms of the disorder. Furthermore, we discuss the potential therapeutic strategies that target these pathological pathways. Elucidating these mechanisms may ultimately advance our understanding of schizophrenia’s etiological foundations and guide the development of curative interventions. Full article

Modern research laboratories are constantly evolving to meet the growing demands for precision, quality, and flexibility in scientific work. The modernization of existing experimental test benches plays a crucial role in improving efficiency, optimizing processes, and ensuring operational safety. This requires updates to their design, experimental methods, data collection, and results recording—all of which provide the foundation for developing new research concepts. An increasing number of innovations are now guided by the principle of minimizing environmental impact. In line with this approach, an innovative modernization of a tube furnace research station was carried out, based on the concepts of sustainable development and the zero-waste philosophy. To enable thermogravimetric analyses of coffee waste, a previously incomplete tube furnace was refurbished using recycled components. The primary objective was to expand the research capabilities of the existing workstation. As part of the modernization, three indicators of reuse efficiency were calculated: the quantitative indicator W_re-use, the mass indicator $W_{re\text{-}use}^{mass}$, and the cost indicator $W_{re\text{-}use}^{value}$. A quantitative index of 78% and a mass index of approximately 76% were achieved, while the economic value of the recovered components accounted for 11% of the total value of the revitalized research station. This strategy significantly reduced waste generation, carbon dioxide emissions, and the consumption of primary raw materials. Full article

Background/Objectives: This article discusses the clinical–surgical relevance of vascular anatomical variations, such as fenestrations—the division of a vessel into multiple channels that subsequently rejoin distally. Although rare in peripheral veins, these variations, which originate from the incomplete condensation of the embryonic capillary plexus, can predispose thrombosis and necessitate preoperative recognition to avert complications during routine procedures. This study aims to report a rare case of dual origin and double fenestration of the cephalic vein. Methods: During a cadaveric dissection, a variation of the cephalic vein was identified. Results: In this case, an origin of the cephalic vein was observed arising from the dorsal venous network of the hand. It exhibited a double fenestration in the forearm, where a branch of the medial cutaneous nerve of the forearm perforated it before draining into the brachial vein. The second, a proximal origin, arose from the convergence of two tributaries—one originating from the subcutaneous tissue lateral to the brachial muscle and the other from the biceps brachii muscle, forming a single trunk that drained into the subclavian vein. Conclusions: This rare variation of the cephalic vein (dual origin and fenestration) carries significant hemodynamic implications, including an increased risk of turbulence and thrombosis. The atypical anatomical relationship between the nerve and the fenestrated vein also heightens the potential for iatrogenic injuries. In-depth knowledge of such anomalies is crucial for healthcare professionals to minimize complications and optimize the success of procedures like venous access and arteriovenous fistulas, ultimately ensuring patient safety. Full article

Lacking effective therapeutics, cholangiocarcinoma (CCA) remains a deadly malignancy of the biliary tract. The Hippo pathway effector protein Yes-associated protein (YAP) is implicated in CCA pathogenesis and chemotherapeutic resistance; however, the oncogenic mechanisms underlying YAP regulation remain incompletely understood. An enhanced understanding of YAP and its role in CCA may uncover novel therapeutic targets and better define resistance pathways. Human CCA cells and murine syngeneic CCA models were utilized to explore the molecular relationship of YAP and protein tyrosine phosphatase 1B (PTP1B). Previous work in CCA has demonstrated that YAP interacts with multiple protein tyrosine phosphatases, including SHP2 and PTP1B. We observed that PTP1B pharmacologic inhibition was associated with increased cell proliferation and YAP target gene expression, while genetically enforced overexpression of PTP1B was associated with a decrease in YAP activation. Treatment of CCA cells in vitro and syngeneic, orthotopically implanted CCA murine tumors in vivo with standard cytotoxic chemotherapy, gemcitabine/cisplatin, had enhanced efficacy in the setting of PTP1B overexpression. These findings demonstrate that pYAP^Y357 can be modulated through protein tyrosine 1B phosphatase activity, and reducing pYAP^Y357 through enhanced phosphatase levels can sensitize CCA to chemotherapy. Full article

Organoid technology has emerged as a revolutionary tool in cancer research, offering physiologically accurate, three-dimensional models that preserve the histoarchitecture, genetic stability, and phenotypic complexity of primary tumors. These self-organizing structures, derived from adult stem cells, induced pluripotent stem cells, or patient tumor biopsies, recapitulate critical aspects of tumor heterogeneity, clonal evolution, and microenvironmental interactions. Organoids serve as powerful systems for modeling tumor progression, assessing drug sensitivity and resistance, and guiding precision oncology strategies. Recent innovations have extended organoid capabilities beyond static culture systems. Integration with microfluidic organoid-on-chip platforms, high-throughput CRISPR-based functional genomics, and AI-driven phenotypic analytics has enhanced mechanistic insight and translational relevance. Co-culture systems incorporating immune, stromal, and endothelial components now permit dynamic modeling of tumor–host interactions, immunotherapeutic responses, and metastatic behavior. Comparative analyses with conventional platforms, 2D monolayers, spheroids, and patient-derived xenografts emphasize the superior fidelity and clinical potential of organoids. Despite these advances, several challenges remain, such as protocol variability, incomplete recapitulation of systemic physiology, and limitations in scalability, standardization, and regulatory alignment. Addressing these gaps with unified workflows, synthetic matrices, vascularized and innervated co-cultures, and GMP-compliant manufacturing will be crucial for clinical integration. Proactive engagement with regulatory frameworks and ethical guidelines will be pivotal to ensuring safe, responsible, and equitable clinical translation. With the convergence of bioengineering, multi-omics, and computational modeling, organoids are poised to become indispensable tools in next-generation oncology, driving mechanistic discovery, predictive diagnostics, and personalized therapy optimization. Full article

Respiratory syncytial virus (RSV) is a major cause of severe respiratory infections in infants, the elderly, and immunocompromised persons. Innate immune responses to RSV, which are crucial for containment of the infection yet may also be linked to severe disease, are well-studied in the main RSV target cells, respiratory epithelial cells, but the role of pulmonary macrophages (MΦs), key innate immune regulators, remains incompletely defined. This review addresses the interaction of RSV with MΦ, discussing the susceptibility of these cells to productive infection, and MΦ responses to RSV, including cytokine and chemokine release and inflammasome activation. Furthermore, factors contributing to variability in MΦ infectivity and responses, such as MΦ polarization, age, differences in RSV isolates, co-infections, and prior innate priming, are presented. Finally, the review highlights discrepancies observed across experimental models, MΦ origins, and RSV isolates used, complicating the interpretation of MΦ-RSV interactions, thereby underscoring the need for standardized methodologies. Full article