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Pupil and eyeblink response abnormalities during emotional conflict processing in late-life depression
No full text[[abstract]]Introduction This study aims to investigate the locus coeruleus-norepinephrine system (LC-NE) function in late-life depression (LLD) patients by examining task-evoked pupil dilation in the emotional face-word Stroop task, given the recently established coupling between task-evoked pupil dilation and LC-NE activation.Materials and Methods Using video-based eye-tracking and principal component analysis, we explored task-evoked pupil responses and eye blinks in LLD patients (N = 25) and older healthy controls (CTRL) (N = 29) to determine whether there were alterations in pupil responses and eye blinks in LLD compared to CTRL.Results LLD patients exhibited significantly different pupil and eye-blink behavior compared to CTRL, with dampened task-evoked pupil dilation associated with emotional congruency and valence processing mediated by the sympathetic system compared to CTRL. Eye-blink rates associated with emotional valence were also altered in LLD compared to CTRL Moreover, Geriatric Depression Scale-15 scores in LLD correlated with emotional congruency effects revealed by task-evoked pupil dilation.Conclusion The findings demonstrate that LLD patients display altered pupil behavior compared to CTRL. These altered responses correlated with the severity of depressive symptoms, indicating their potential as objective biomarkers for use in large at-risk populations for LLD
Loneliness modulates the neural dynamics of language processing in healthy older adults: Evidence from event-related potentials
No full text[[abstract]]Loneliness, a distressing emotional response to perceived deficiencies in social interactions, has seen a marked increase in prevalence since the Covid-19 pandemic. While previous research has linked loneliness in older adults to affective disorders and cognitive decline, its impact on language comprehension-a crucial aspect of social interaction-remains underexplored. This study addresses this gap by examining the effects of loneliness on semantic retrieval in healthy older adults. Using event-related potentials, we measured participants' neural responses as they verified category membership across three conditions: high typicality, low typicality, and category violations. We found that loneliness was negatively correlated with an N400 amplitude reduction for low-typicality items compared to category violations. Moreover, individuals who reported a high level of loneliness exhibited attenuated and delayed N400 effects within more restricted time windows compared to their less lonely counterparts. These results indicate that loneliness impairs semantic memory retrieval in older adults, potentially compromising language comprehension and further exacerbating social isolation. This research highlights the detrimental impact of loneliness on linguistic abilities, which may contribute to a vicious cycle of increasing social isolation and deepening loneliness
[[alternative]]新冠肺炎疫情衝擊下醫院環境作業安全之影響
No full text[[abstract]]Objectives: COVID-19 had a major effect on hospital environmental safety, leading to an increase in workplace accidents and hazards. This study explored the hazardous factors that compromised hospital environmental safety during the pandemic. Methods: This study was conducted at a large medical center in northern Taiwan. Data from environmental safety inspections and hospital premises were used to compare safety inspection outcomes before and during the COVID-19 outbreak. Statistical analyses were conducted using an analysis of variance and a generalized estimating equation model for repeated measures. Results: When the levels of domestic COVID-19 alerts increased, an increase was observed in the deficiency rates for “electricity safety and facilities” and “flammable materials management.” By contrast, the deficiency rate for “emergency response” decreased. Additionally, the emergency department demonstrated lower performance in environmental safety management compared with the intensive care units and operating rooms, underscoring the need for department-specific considerations in safety management. Conclusions: Environmental safety inspections are essential for identifying potential hazards in hospitals. In cases of future outbreaks of infectious diseases, hospitals should prioritize monitoring the use of flammable alcohol-based hand sanitizers, ensuring electrical safety, monitoring hospital entrances and evacuation routes, and managing changes in temporary measures. These efforts are essential for fostering a safer health-care environment
Smart healthcare and IoMT: Best practices and perspectives of AI and ML
No full text[[abstract]]The healthcare sector has witnessed rapid advancements aimed at providing improved health services and enhanced patient care. These developments encompass cutting-edge technologies, including wearable devices, medical sensors, and internet-connected medical equipment. Such innovations play a crucial role in remotely monitoring and tracking patients’ conditions, offering a more efficient alternative to manual data recording. Collectively referred to as the Internet of Medical Things (IoMT), these applications represent the integration of Internet of Things (IoT) technologies within the medical field. From our perspective, the current state of smart healthcare can be further enhanced, especially given the ongoing developments in artificial intelligence (AI) and machine learning (ML). By leveraging the data collected from devices in the IoMT, we have the opportunity to integrate AI and ML technologies. This integration enables us to utilize the gathered data effectively, thereby contributing to the improvement of a smart healthcare system. In conclusion, we are going to show how the implementation of AI or ML together with IoMT, we can develop even more advanced smart healthcare, from predicting early disease or giving suggestions for the best treatment for patient conditions. © 2025 selection and editorial matter, Hiren Kumar Thakkar, Chintan Bhatt, Victor C.M. Leung and Ilangko Balasingham; individual chapters, the contributors
Bimetallic photonanozyme catalysts for fluorometric analysis of total antioxidant capacity in human saliva
No full text[[abstract]]Oxidative stress, resulting from an imbalance between free radicals and antioxidants, is widely recognized as a critical factor in numerous human disorders, including neurodegenerative disorders and cancers. Evaluating total antioxidant capacity (TAC) in bodily fluids is a vital bioanalytical parameter for assessing oxidative stress and redox status. However, current methods for TAC evaluation are significantly limited by their inability to detect a wide range of antioxidant molecules, their lack of sensitivity to important thiol antioxidants, and their high cost and complexity. In this study, we develop bimetallic gold-silver nanoclusters (AuAgNCs) as a photocatalyst for the evaluation of TAC. The reported nanozyme exhibits strong oxidase-like activity and precise, stable photocatalytic performance under LED irradiation. Upon light exposure, the bimetallic nanoclusters generate reactive oxygen species (ROS) by utilizing dissolved oxygen. These generated ROS then oxidize a non-fluorescent substrate, thiamine, to its fluorescent form, thiochrome. In the presence of antioxidants, ROS scavenging inhibits this conversion resulting in a lower fluorescence signal. This capability enables the detection of all physiologically relevant antioxidant species by responding to both single electron transfer (SET) and hydrogen atom transfer (HAT) reactions, allowing for the detection of a broad range of antioxidants present in saliva. This approach highlights the potential of innovative nanostructures like bimetallic photonanozymes in advancing future diagnostic and therapeutic strategies for oxidative stress-related disorders
High sensitivity mercury ion detection via thermal shock and quench with molecular sieve-functionalized FETs
No full text[[abstract]]This study developed a molecular sieve-based mercury ion sensor utilizing an extended-gate field-effect transistor (EGFET) and introduced a thermal shock and quench strategy to significantly enhance detection sensitivity. Molecular sieves, which are cyclic molecules with a high affinity for specific ions, were employed in this strategy, designed based on their thermal properties and structural stability. Thermal shock was utilized to accelerate reaction kinetics and overcome activation energy barriers, while subsequent thermal quenching stabilized the resulting complexes. This approach improved the detection limit by four orders of magnitude, achieving an ultimate detection limit of 2.5 pM Hg2+. Notably, DNA linker with optical properties was used as a surfaceanchoring connector molecule. The DNA was easily modified with functional groups and fluorophores, enhancing its ability to monitor surface modification processes and facilitating efficient interactions with molecules, antibodies, and surfaces. Fluorescence quenching was observed during interactions between DNA and the molecular sieve, enabling precise monitoring of surface quality and providing an innovative platform for biosensor development. Furthermore, by creating a single-layer structure on the surface, this study enabled rapid detection through direct modulation of the electrical double layer. Lastly, the study evaluated the selectivity of the molecular sieve toward various metal ions. The results demonstrated that the structural stability and thermal properties of the molecular sieve play a critical role in sensor sensitivity. These characteristics are vital for sensor performance and must be carefully considered during the sensor design to optimize the application efficiency
Effect of environmental factors on postoperative recurrent primary spontaneous pneumothorax: A case-crossover study
No full text[[abstract]]Objective Surgery is one of the preferred primary treatments for primary spontaneous pneumothorax (PSP); however, postoperative recurrent pneumothorax (PORP), defined as recurrence on the same side, occurs in 3-13% of cases. While environmental factors have been implicated in PSP occurrence, their role in PORP remains unclear. This study aimed to investigate the impact of environmental factors on the onset of PSP and PORP in the same patient population. Methods Between 2009 and 2019, a total of 442 patients (aged <= 40 years) underwent 486 surgeries for PSP, with 43 patients (8.8%) experiencing a first PORP. Management of PORP included reoperation (29 patients), pleural drainage with chemical pleurodesis (4 patients), and conservative observation (10 patients). In this case-crossover study, the day of symptom onset for PSP and PORP was designated as the "case day." To evaluate potential lag effects, the days leading up to symptom onset, ranging from 1 day prior (lag day 1) to 7 days prior (lag day 7), were also analyzed as "case days." Unidirectional matched control days were selected 14-21 days before the case day (lag day 0). Results Elevated PM2.5 levels were significantly associated with PSP onset at lag day 0 and lag day 1, with increased odds observed at these time points (p = 0.04 and p = 0.02, respectively). No such association was found for PORP patients. Meteorological factors did not appear to influence PSP or PORP risk. Seasonally, both the PSP incidence and the PORP incidence were significantly greater in autumn and spring than in summer and winter (p < 0.001). Conclusion PSP and PORP demonstrate seasonal clustering, with higher incidences in autumn and spring. Elevated PM2.5 levels appear to contribute to PSP onset but not PORP, suggesting that air pollution may be a potential trigger for PSP. Further research is needed to clarify environmental influences and optimize tailored management strategies
Transcriptome insights into protective mechanisms of ferroptosis inhibition in aortic dissection
No full text[[abstract]]Aortic dissection (AD) is a life-threatening vascular condition with limited pharmacological options, and shared risk factors with cardiac disease include hypertension, atherosclerosis, smoking, and dyslipidemia. This study investigated Ferrostatin-1 (Fer-1), a ferroptosis inhibitor, in a BAPN/Ang-II-induced mouse model of AD, revealing significant therapeutic potential. Fer-1 significantly reduced AD incidence and mortality by preserving aortic wall integrity. RNA sequencing identified 922 differentially expressed genes, with 416 upregulated and 506 downregulated. Bioinformatics analysis revealed that Fer-1 modulates key regulators, such as MEF2C and KDM5A, impacting immune responses, oxidative stress, apoptosis, and lipid metabolism. Additionally, Fer-1 alters miRNA expression, with the upregulation of miR-361-5p and downregulation of miR-3151-5p, targeting pathways involved in inflammation, oxidative stress, and smooth muscle cell (SMC) phenotypic stability. Functional pathway analysis highlighted the inhibition of actin cytoskeleton, ILK, and IL-17 signaling, essential for SMC differentiation and extracellular matrix remodeling. Gene interaction network analysis identified 21 central molecules, including CXCR3, ACACA, and BPGM, associated with lipid metabolism, inflammation, and vascular remodeling. This research elucidates the mechanism of ferroptosis in AD pathogenesis and establishes Fer-1 as a promising therapeutic intervention. AD and cardiac diseases share molecular mechanisms, risk factors, and pathological processes, positioning AD within the broader scope of cardiovascular pathology. By attenuating lipid peroxidation, oxidative stress, and inflammation, Fer-1 may have cardioprotective effects beyond AD, providing a foundation for future translational research in cardiovascular medicine
Plasminogen deficiency reduces disease severity and immune responses in enterovirus A71-infected mice
No full text[[abstract]]Enterovirus A71 (EV-A71) is a causative agent of hand, foot, and mouth diseases. EV-A71 infections may result in severe neurological complications in children. Although several receptors or attachment molecules for EV-A71 have been identified, EV-A71 can still infect host cells even after blocking these receptors with antibodies. We have previously identified plasminogen (PLG), a circulating zymogen of plasmin, as a cell membrane-associated EV-A71-interacting glycoprotein. We confirmed that anti-PLG antibodies could reduce the binding of EV-A71 to RD cells as anti-SCARB2 and anti-nucleolin. Knockdown of PLG reduced EV-A71 binding to RD cells, and preincubation of PLG with EV-A71 increased virus binding. Enzyme-linked immunosorbent assay and surface plasmon resonance assays demonstrated the direct binding of PLG to EV-A71. We further evaluated the biological characteristics of EV-A71-infected PLG knockout (heterozygous) and wild-type mice. We found that the clinical scores and mortality of WT mice were higher than those of PLG-knockout mice after EV-A71 infection. The viral loads in the spinal cord of PLG knockout mice were lower than those in WT mice 6 days post-infection. EV-A71-associated cytokines such as IL-1 beta, IL-6, MCP-1, IL-10, and IFN-gamma were investigated. Serum IL-10 and MCP-1 expression were significantly higher in EV-71-infected WT mice than in PLG knockout mice, and MCP-1 may be one of the critical chemokines that induce intense inflammation and chemoattracts leukocytes. Our findings reveal a possible role for PLG in EV-A71 infection/pathogenesis and shed light on developing novel therapeutic approaches and drugs to prevent EV-A71 infection.IMPORTANCEUnderstanding the pathogenesis of enterovirus A71 (EV-A71) for developing novel drugs or therapeutic approaches has always been a significant issue. In this study, we demonstrated the interactions between plasminogen (PLG) and EV-A71, characterized the biological effects of EV-A71-infected PLG knockout mice, and evaluated their immune response. We found that EV-A71 caused more severe tissue damage than PLG knockout mice in skeletal muscle, spinal cord, and brain stem. Higher virus protein was observed in these tissues of WT mice. The reduced clinical scores, mortality, and cytokine expression suggested PLG may be involved in EV-A71 infection-induced cytokine storm. The findings and animal model in the current study provide the new drug target for anti-EV-A71 drug discovery
Palmitic acid and lipopolysaccharide induce macrophage TNFα secretion, suppressing browning regulators and mitochondrial respiration in adipocytes
No full text[[abstract]]Obesity and its associated pro-inflammatory activity contribute significantly to metabolic dysfunction. In contrast, browning of white adipose tissue (WAT) generally improves metabolic health. Our prior research suggested that macrophage-derived pro-inflammatory cytokines suppress key regulators of browning-adrenergic receptor beta 3 (Adrb3) and peroxisome proliferator-activated receptor gamma (Pparg)-as well as energy metabolism mediators-insulin receptor substrate 1 (Irs1) and hormone-sensitive lipase (Lipe)-in dietinduced obese mice. To explore this mechanism, we developed an in vitro model using RAW264.7 macrophages and 3T3-L1 adipocytes exposed to palmitic acid (PA) and/or lipopolysaccharide (LPS). PA (200 mu M) and LPS (1.0 mu g/ml) synergistically promoted M1 polarization of macrophages and secretion of pro-inflammatory cytokines, with tumor necrosis factor-alpha (TNF alpha), C-C motif chemokine ligand 2 (CCL2), CCL5, and interleukin6 (IL-6) being predominant. Conditioned media from both control and PA-treated macrophages, when exposed to LPS >= 0.01 mu g/ml, significantly downregulated Adrb3, Pparg, Irs1, and Lipe in adipocytes. At physiologically relevant LPS levels (<= 0.001 mu g/ml), PA-treated macrophage media exerted greater suppression of these genes than controls. Among the cytokines, TNF alpha emerged as the primary mediator, significantly reducing expression of the four key regulators. Furthermore, adipocytes treated with TNF alpha exhibited significant reductions in both uncoupling protein 1 (Ucp1) expression and mitochondrial respiration. These findings demonstrate that exposure to obesity-associated factors (PA and LPS) induces macrophage-derived TNF alpha, which suppresses browning and mitochondrial function in adipocytes. This mechanism may inform new therapeutic strategies targeting TNF alpha to alleviate obesity-related metabolic disorders