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In this study, we optimized the parameters of diffusion bonding on multi-layered stainless steel 316L and 430 stacks. The preparation process for diffusion bonding is crucial, as the bonding surfaces need to be polished and meticulously cleaned to ensure a smooth bonding process. We fabricated twelve-layer plates consisting of 55 mm × 55 mm × 3 mm and 100 mm × 50 mm × 3 mm dimensions, and the bonding response was investigated by evaluating the tensile strength of the bonding zone under varying bonding conditions, with a bonding temperature ranging from 1000 to 1048 °C, a bond time ranging from 15 to 60 min, pressure ranging from 10 to 25.3 MPa, and under a vacuum environment. SS430 exhibits a significantly higher compression creep rate than SS316L. The compressibility of diffusion welding materials does not impact the diffusion bonding strength. Multi-axial tensile strength tests confirmed strong bonding joint strength in various axes. The tensile strengths of monolithic and Diffusion bonding (DB) specimens tested in parallel are essentially identical. The optimized diffusion bonding parameters (Condition G2C: 1048 °C/25.3 MPa/15 min) are ideal for producing SS316L stainless steel cores in compact heat exchangers, offering a superior bonding quality and reduced costs. These findings have practical implications for the production of stainless steel cores in compact heat exchangers, demonstrating the relevance and applicability of our research.
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The effects of dry-salted and salt-fermented processing on the physicochemical characteristics and microbial communities of Yacai were systematically investigated. The results showed that the contents of total acid, amino acid nitrogen (AAN) and nitrite in the final products of dry-salted Yacai were greater than those in salt-fermented Yacai. Lactic acid was the dominant organic acid in the two types of Yacai. Dry-salted processing is more conducive to forming a high-quality reddish-brown color. During whole pickling process, the microbial diversity of dry-salted Yacai was higher than that of salt-fermented Yacai, particularly in the early and middle stages of fermentation. For dry-salted Yacai, 8 bacteria (Natribacillus, Chromohalobacter, Marinococcus, Lentibacillus, Nesterenkonia, Gracilibacillus, Oceanobacillus and Tetragenococcus) and 1 fungus (Zygosaccharomyces) showed a significant positive correlation with AAN. For salt-fermented Yacai, 8 bacteria (Gracilibacillus, Alkalibacillus, Oceanobacillus, Virgibacillus, Lentibacillus, Salibacterium, Chromohalobacter and Tetragenococcus) and 3 fungi (Zygosaccharomyces, Millerozyma, and Wickerhamomyces) exhibited significant positive correlations with AAN.
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Samples of ambient volatile organic compounds ï¼VOCsï¼ were collected using SUMMA canisters at three Country Control Sites in Shijiazhuang during the spring of 2019, 2021, and 2022, which were detected using gas chromatography/mass spectrometry ï¼GC/MSï¼. To investigate the characteristics and temporal variations of VOCs mass concentration levels, the online monitoring data of ozone ï¼O3ï¼ and PM2.5 at the same site were also collected. Subsequently, the ozone formation potential ï¼OFPï¼ and secondary organic aerosol formation potential ï¼SOAFPï¼ were utilized to assess the chemical activity of VOCs. Additionally, the potential source areas of VOCs in spring in Shijiazhuang were further identified using the potential source contribution factor ï¼PSCFï¼ method and concentration weight trajectory analysis ï¼CWTï¼. Hence, the major VOCs sources were evaluated with the VOCs initial mixing ratio. The results demonstrated that the averaged concentration of VOCs during the polluted period and clean period of spring in Shijiazhuang were 191.17 µg·m-3 and 122.18 µg·m-3, respectively. Meanwhile, the OFP was 361.23 µg·m-3 during the polluted period and 266.96 µg·m-3 during the clean period, whereas the SOAFP was 1.98 µg·m-3 and 1.61 µg·m-3, respectively. Therefore, effective control of benzene, toluene, ethylbenzene, and xylene ï¼BTEXï¼ is crucial for reducing PM2.5 and O3 pollution. Based on the results obtained from weight PSCF and CWT, the potential source areas of VOCs were further identified to be primarily located in the eastern Yuhua District, the high-tech district, and the northern Luancheng District of Shijiazhuang. These areas were influenced not only by local emissions but also by transport from neighboring regions, in which consistency between the CWT and PSCF results further supported these findings. Furthermore, the results obtained from the benzene/toluene/ethylbenzene ï¼B/T/Eï¼ and xylene/benzene ï¼X/Bï¼ ratios indicated that the main sources of VOCs in Shijiazhuang in spring were vehicle exhaust sources and burning sources, leading to a more serious air mass aging phenomenon. Hence, controlling vehicle emissions and implementing regional cooperative measures are the effective strategies for optimizing the air quality of Shijiazhuang.
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The lymphatic system is the same reticular fluid system as the circulatory system found throughout the body in vascularized tissues. Lymphatic vessels are low-pressure, blind-ended tubular structures that play a crucial role in maintaining tissue fluid homeostasis, immune cell transport, and lipid absorption. The heart also has an extensive lymphatic network, and as research on cardiac lymphatics has progressed in recent years, more and more studies have found that cardiac lymphangiogenesis may ameliorate certain cardiovascular diseases, and therefore stimulation of cardiac lymphangiogenesis may be an important tool in the future treatment of cardiovascular diseases. This article briefly reviews the development and function of cardiac lymphatic vessels, the interaction of cardiac lymphatic vessels with cardiovascular diseases (including atrial fibrillation, coronary atherosclerosis, and heart failure), and finally discusses the therapeutic potential of targeted cardiac lymphatic therapy for cardiovascular diseases.
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The tumor microenvironment (TME) plays a pivotal role in the onset, progression, and treatment response of cancer. Among the various components of the TME, cancer-associated fibroblasts (CAFs) are key regulators of both immune and non-immune cellular functions. Leveraging single-cell RNA sequencing (scRNA) data, we have uncovered previously hidden and promising roles within this specific CAF subgroup, paving the way for its clinical application. However, several critical questions persist, primarily stemming from the heterogeneous nature of CAFs and the use of different fibroblast markers in various sample analyses, causing confusion and hindrance in their clinical implementation. In this groundbreaking study, we have systematically screened multiple databases to identify the most robust marker for distinguishing CAFs in lung cancer, with a particular focus on their potential use in early diagnosis, staging, and treatment response evaluation. Our investigation revealed that COL1A1, COL1A2, FAP, and PDGFRA are effective markers for characterizing CAF subgroups in most lung adenocarcinoma datasets. Through comprehensive analysis of treatment responses, we determined that COL1A1 stands out as the most effective indicator among all CAF markers. COL1A1 not only deciphers the TME signatures related to CAFs but also demonstrates a highly sensitive and specific correlation with treatment responses and multiple survival outcomes. For the first time, we have unveiled the distinct roles played by clusters of CAF markers in differentiating various TME groups. Our findings confirm the sensitive and unique contributions of CAFs to the responses of multiple lung cancer therapies. These insights significantly enhance our understanding of TME functions and drive the translational application of extensive scRNA sequence results. COL1A1 emerges as the most sensitive and specific marker for defining CAF subgroups in scRNA analysis. The CAF ratios represented by COL1A1 can potentially serve as a reliable predictor of treatment responses in clinical practice, thus providing valuable insights into the influential roles of TME components. This research marks a crucial step forward in revolutionizing our approach to cancer diagnosis and treatment.
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Biomarcadores Tumorais , Fibroblastos Associados a Câncer , Carcinoma Pulmonar de Células não Pequenas , Neoplasias Pulmonares , Microambiente Tumoral , Humanos , Neoplasias Pulmonares/mortalidade , Neoplasias Pulmonares/patologia , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/diagnóstico , Neoplasias Pulmonares/terapia , Carcinoma Pulmonar de Células não Pequenas/mortalidade , Carcinoma Pulmonar de Células não Pequenas/patologia , Carcinoma Pulmonar de Células não Pequenas/genética , Carcinoma Pulmonar de Células não Pequenas/diagnóstico , Fibroblastos Associados a Câncer/metabolismo , Fibroblastos Associados a Câncer/patologia , Biomarcadores Tumorais/metabolismo , Prognóstico , Regulação Neoplásica da Expressão GênicaRESUMO
BACKGROUND: The heightened risk of cardiovascular and cerebrovascular events is associated with the increased instability of atherosclerotic plaques. However, the lack of effective diagnostic biomarkers has impeded the assessment of plaque instability currently. This study was aimed to investigate and identify hub genes associated with unstable plaques through the integration of various bioinformatics tools, providing novel insights into the detection and treatment of this condition. METHODS: Weighted Gene Co-expression Network Analysis (WGCNA) combined with two machine learning methods were used to identify hub genes strongly associated with plaque instability. The cell-type identification by estimating relative subsets of RNA transcripts (CIBERSORT) method was utilized to assess immune cell infiltration patterns in atherosclerosis patients. Additionally, Gene Set Variation Analysis (GSVA) was conducted to investigate the potential biological functions, pathways, and mechanisms of hub genes associated with unstable plaques. To further validate the diagnostic efficiency and expression of the hub genes, immunohistochemistry (IHC), quantitative real-time polymerase chain reaction (RT-qPCR), and enzyme-linked immunosorbent assay (ELISA) were performed on collected human carotid plaque and blood samples. Immunofluorescence co-staining was also utilized to confirm the association between hub genes and immune cells, as well as their colocalization with mitochondria. RESULTS: The CIBERSORT analysis demonstrated a significant decrease in the infiltration of CD8 T cells and an obvious increase in the infiltration of M0 macrophages in patients with atherosclerosis. Subsequently, two highly relevant modules (blue and green) strongly associated with atherosclerotic plaque instability were identified. Through intersection with mitochondria-related genes, 50 crucial genes were identified. Further analysis employing least absolute shrinkage and selection operator (LASSO) logistic regression and support vector machine recursive feature elimination (SVM-RFE) algorithms revealed six hub genes significantly associated with plaque instability. Among them, NT5DC3, ACADL, SLC25A4, ALDH1B1, and MAOB exhibited positive correlations with CD8 T cells and negative correlations with M0 macrophages, while kynurenine 3-monooxygenas (KMO) demonstrated a positive correlation with M0 macrophages and a negative correlation with CD8 T cells. IHC and RT-qPCR analyses of human carotid plaque samples, as well as ELISA analyses of blood samples, revealed significant upregulation of KMO and MAOB expression, along with decreased ALDH1B1 expression, in both stable and unstable samples compared to the control samples. However, among the three key genes mentioned above, only KMO showed a significant increase in expression in unstable plaque samples compared to stable plaque samples. Furthermore, the expression patterns of KMO in human carotid unstable plaque tissues and cultured mouse macrophage cell lines were assessed using immunofluorescence co-staining techniques. Finally, lentivirus-mediated KMO silencing was successfully transduced into the aortas of high-fat-fed ApoE-/- mice, with results indicating that KMO silencing attenuated plaque formation and promoted plaque stability in ApoE-/- mice. CONCLUSIONS: The results suggest that KMO, a mitochondria-targeted gene associated with macrophage cells, holds promise as a valuable diagnostic biomarker for assessing the instability of atherosclerotic plaques.
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Placa Aterosclerótica , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Biologia Computacional/métodos , Perfilação da Expressão Gênica , Redes Reguladoras de Genes , Genes Mitocondriais/genética , Macrófagos/metabolismo , Macrófagos/patologia , Mitocôndrias/metabolismo , Placa Aterosclerótica/genética , Placa Aterosclerótica/patologia , Reprodutibilidade dos Testes , Quinurenina 3-Mono-Oxigenase/genética , Quinurenina 3-Mono-Oxigenase/metabolismoRESUMO
The practical implementation of lithium-sulfur batteries is severely hindered by the rapid capacity fading due to the solubility of the intermediate lithium polysulfides (LiPSs) and the sluggish redox kinetics. Herein, high-entropy metal nitride nanocrystals (HEMN) embedded within nitrogen-doped concave porous carbon (N-CPC) polyhedra are rationally designed as a sulfur host via a facile zeolitic imidazolate framework (ZIF)-driven adsorption-nitridation process toward this challenge. The configuration of high-entropy with incorporated metal manganese (Mn) and chromium (Cr) will optimize the d-band center of active sites with more electrons occupied in antibonding orbitals, thus promoting the adsorption and catalytic conversion of LiPSs. While the concave porous carbon not only accommodates the volume change upon the cycling processes but also physically confines and exposes active sites for accelerated sulfur redox reactions. As a result, the resultant HEMN/N-CPC composites-based sulfur cathode can deliver a high specific capacity of 1274 mAh g-1 at 0.2 C and a low capacity decay rate of 0.044% after 1000 cycles at 1 C. Moreover, upon sulfur loading of 5.0 mg cm-2, the areal capacity of 5.0 mAh cm-2 can still be achieved. The present work may provide a new avenue for the design of high-performance cathodes in Li-S batteries.
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Metal halide materials have recently drawn increasing research interest for their excellent opto-electronic properties and structural diversity, but their resulting rigid structures render them brittle and poor formability during manufacturing. Here we demonstrate a thermoplastic luminant hybrid lead halide solid by integrating lead bromide complex into tri-n-octylphosphine oxide (TOPO) matrix. The construction of the hybrid materials can be achieved by a simple dissolution process, in which TOPO molecules act as the solvents and ligands to yield the monodispersed clusters. The combination of these functional units enables the near-room-temperature melt-processing of the materials into targeted geometry by simple molding or printing techniques, which offer possibilities for fluorescent writing inks with outstanding self-healing capacity to physical damage. The intermarriage between metal halide clusters with functional molecules expands the range of practical applications for hybrid metal halide materials.
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Atherosclerosis (AS) is the formation of atherosclerotic plaques on the walls of the arteries, causing them to narrow. If this occurs in the coronary arteries, the blood vessels may be completely blocked, resulting in myocardial infarction; if it occurs in the blood vessels of the brain, the blood vessels may be blocked, resulting in cerebral infarction, i.e., stroke. Studies have shown that the pathogenesis of atherosclerosis involves the processes of inflammation, lipid infiltration, oxidative stress, and endothelial damage, etc. SIRT, as a key factor regulating the molecular mechanisms of oxidative stress, inflammation, and aging, has an important impact on the pathogenesis of plaque formation, progression, and vulnerability. Statistics show that AS accounts for about 50 per cent of deaths in Western countries. Currently, oral medication is the mainstay of AS treatment, but its development is limited by side effects, low bioavailability and other unfavourable factors. In recent years, with the rapid development of nano-preparations, researchers have combined statins and natural product drugs within nanopreparations to improve their bioavailability. Based on this, this paper summarises the main pathogenesis of AS and also proposes new oral nanoformulations such as liposomes, nanoparticles, nanoemulsions, and nanocapsules to improve their application in the treatment of AS.
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Transition metal chalcogenides have been identified as low-cost and efficient electrocatalysts to promote the hydrogen evolution reaction in alkaline media. However, the identification of active sites and the underlying catalytic mechanism remain elusive. In this work, we employ operando X-ray absorption spectroscopy and near-ambient pressure X-ray photoelectron spectroscopy to elucidate that NiS undergoes an in-situ phase transition to an intimately mixed phase of Ni3S2 and NiO, generating highly active synergistic dual sites at the Ni3S2/NiO interface. The interfacial Ni is the active site for water dissociation and OH* adsorption while the interfacial S acts as the active site for H* adsorption and H2 evolution. Accordingly, the in-situ formation of Ni3S2/NiO interfaces enables NiS electrocatalysts to achieve an overpotential of only 95 ± 8 mV at a current density of 10 mA cm-2. Our work highlighted that the chemistry of transition metal chalcogenides is highly dynamic, and a careful control of the working conditions may lead to the in-situ formation of catalytic species that boost their catalytic performance.
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The MobileNetV3-based improved sine-cosine algorithm (ISCA-MobileNetV3) was combined with an artificial olfactory sensor (AOS) to address the redundancy in olfactory arrays, thereby achieving low-cost and high-precision detection of mycotoxin-contaminated maize. Specifically, volatile organic compounds of maize interacted with unoptimized AOS containing eight porphyrins and eight dye-attached nanocomposites to obtain the scent fingerprints for constructing the initial data set. The optimal decision model was MobileNetV3, with more than 98.5% classification accuracy, and its output training loss would be input into the optimizer ISCA. Remarkably, the number of olfactory arrays was reduced from 16 to 6 by ISCA-MobileNetV3 with about a 1% decrease in classification accuracy. Additionally, the developed system showed that each online evaluation was less than one second on average, demonstrating outstanding real-time performance for ensuring food safety. Therefore, AOS combined with ISCA-MobileNetV3 will encourage the development of an affordable and on-site platform for maize quality detection.
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Contaminação de Alimentos , Micotoxinas , Zea mays , Zea mays/química , Micotoxinas/análise , Contaminação de Alimentos/análise , Compostos Orgânicos Voláteis/química , AlgoritmosRESUMO
Traumatic perioperative conditions may trigger early systemic responses, activate leukocytes and reprogram the immune system. We hypothesize that leukocyte activation may not revert to pre-surgical states, and that protracted activation may emerge with increased risks of comorbidities. We tested this concept by examining the transcriptomes of monocytes and T cells in a representative observational cohort of patients (n = 13) admitted for elective cardiac surgery. Transcriptomes in T cells and monocytes were compared from before surgery (t0), and monocytes were analyzed longitudinally after acute (t24hr), and convalescent (t3m) time points. Monocytes and T cells expressed distinct transcriptomes, reflected by statistically significant differential expression of 558 T cell related genes. Monocytes expressed genes related to protein degradation and presented atypical activation of surface markers and cytoplasmic functions over time. Additionally, monocytes exhibited limited transcriptomic heterogeneity prior to surgery, and long-term patterns of gene expression associated with atherosclerosis showed three temporally distinct signatures. These data establish that post-cardiac surgery transcriptomes of monocytes differ even at three months compared to baselines, which may reflect latent ('smoldering') inflammation and persistent progression of tissue degenerative processes that should inform clinical care.
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BACKGROUND: Adherens junction in the blood-labyrinth barrier is largely unexplored because it is traditionally thought to be less important than the tight junction. Since increasing evidence indicates that it actually functions upstream of tight junction adherens junction may potentially be a better target for ameliorating the leakage of the blood-labyrinth barrier under pathological conditions such as acoustic trauma. AIMS: This study was conducted to investigate the pathogenesis of the disruption of adherens junction after acoustic trauma and explore potential therapeutic targets. METHODS: Critical targets that regulated the disruption of adherens junction were investigated by techniques such as immunofluorescence and Western blottingin C57BL/6J mice. RESULTS: Upregulation of Vascular Endothelial Growth Factor (VEGF) and downregulation of Pigment Epithelium-derived Factor (PEDF) coactivated VEGF-PEDF/VEGF receptor 2 (VEGFR2) signaling pathway in the stria vascularis after noise exposure. Downstream effector Src kinase was then activated to degrade VE-cadherin and dissociate adherens junction which led to the leakage of the blood-labyrinth barrier. By inhibiting VEGFR2 or Src kinase VE-cadherin degradation and blood-labyrinth barrier leakage could be attenuated but Src kinase represented a better target to ameliorate blood-labyrinth barrier leakage as inhibiting it would not interfere with vascular endothelium repair neurotrophy and pericytes proliferation mediated by upstream VEGFR2. CONCLUSION: Src kinase may represent a promising target to relieve noise-induced disruption of adherens junction and hyperpermeability of the blood-labyrinth barrier.
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In this paper, we have systematically studied the electronic instability of pressured black phosphorous (BP) under strong magnetic field. We first present an effective model Hamiltonian for pressured BP near theLifshitzpoint. Then we show that when the magnetic field exceeds a critical value, the nodal-line semimetal (NLSM) state of BP with a small band overlap re-enters the semiconductive phase by re-opening a small gap. This results in a narrow-bandgap semiconductor with a partially flat valence band edge. Moreover, we demonstrate that above this critical magnetic field, two possible instabilities, i.e. charge density wave phase and excitonic insulator (EI) phase, are predicted as the ground state for high and low doping concentrations, respectively. By comparing our results with the experiment (Sunet al2018Sci. Bull.631539), we suggest that the field-induced instability observed experimentally corresponds to an EI. Furthermore, we propose that the semimetallic BP under pressure with small band overlaps may provide a good platform to study the magneto-exciton insulators. Our findings bring the first insight into the electronic instability of topological NLSM in the quantum limit.
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Intrauterine growth restriction (IUGR), when a fetus does not grow as expected, is associated with a reduction in hepatic functionality and a higher risk for chronic liver disease in adulthood. Utilizing early developmental plasticity to reverse the outcome of poor fetal programming remains an unexplored area. Focusing on the biochemical profiles of neonates and previous transcriptome findings, piglets from the same fetus are selected as models for studying IUGR. The cellular landscape of the liver is created by scRNA-seq to reveal sex-dependent patterns in IUGR-induced hepatic injury. One week after birth, IUGR piglets experience hypoxic stress. IUGR females exhibit fibroblast-driven T cell conversion into an immune-adapted phenotype, which effectively alleviates inflammation and fosters hepatic regeneration. In contrast, males experience even more severe hepatic injury. Prolonged inflammation due to disrupted lipid metabolism hinders intercellular communication among non-immune cells, which ultimately impairs liver regeneration even into adulthood. Additionally, Apolipoprotein A4 (APOA4) is explored as a novel biomarker by reducing hepatic triglyceride deposition as a protective response against hypoxia in IUGR males. PPARα activation can mitigate hepatic damage and meanwhile restore over-expressed APOA4 to normal in IUGR males. The pioneering study offers valuable insights into the sexually dimorphic responses to hepatic injury during IUGR.
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Animais Recém-Nascidos , Modelos Animais de Doenças , Retardo do Crescimento Fetal , Retardo do Crescimento Fetal/metabolismo , Retardo do Crescimento Fetal/genética , Animais , Feminino , Masculino , Suínos , Fígado/metabolismo , Caracteres Sexuais , Gravidez , Hepatopatias/metabolismo , Hepatopatias/genética , HumanosRESUMO
BACKGROUND: Previous in vivo and in vitro studies have demonstrated that estrogen receptor agonist G-1 regulates glucose and lipid metabolism. This study focused on the effects of G-1 on cardiometabolic syndrome and anti-obesity under a high fat diet (HFD). METHODS: Bilateral ovariectomized female mice were fed an HFD for 6 weeks, and treated them with G-1. A cardiomyocyte insulin resistance model was used to simulate the in vivo environment. The main outcome measures were blood glucose, body weight, and serum insulin levels to assess insulin resistance, while cardiac function and degree of fibrosis were assessed by cardiac ultrasound and pathological observations. We also examined the expression of p-AMPK, p-AKT, and GLUT4 in mice hearts and in vitro models to explore the mechanism by which G-1 regulates insulin signaling. RESULTS: G-1 reduced body weight in mice on an HFD, but simultaneously increased blood glucose and promoted insulin resistance, resulting in myocardial damage. This damage included disordered cardiomyocytes, massive accumulation of glycogen, extensive fibrosis of the heart, and thickening of the front and rear walls of the left ventricle. At the molecular level, G-1 enhances gluconeogenesis and promotes glucose production by increasing the activity of pyruvate carboxylase (PC) while inhibiting GLUT4 translocation via the AMPK/TBC1D1 pathway, thereby limiting glucose uptake. CONCLUSION: Despite G-1's the potential efficacy in weight reduction, the concomitant induction of insulin resistance and cardiac impairment in conjunction with an HFD raises significant concerns. Therefore, comprehensive studies of its safety profile and effects under specific conditions are essential prior to clinical use.
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Dieta Hiperlipídica , Resistência à Insulina , Camundongos Endogâmicos C57BL , Ovariectomia , Receptores Acoplados a Proteínas G , Animais , Feminino , Camundongos , Dieta Hiperlipídica/efeitos adversos , Transportador de Glucose Tipo 4/metabolismo , Insulina/metabolismo , Insulina/sangue , Miócitos Cardíacos/metabolismo , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/patologia , Receptores de Estrogênio/efeitos dos fármacos , Receptores de Estrogênio/metabolismo , Receptores Acoplados a Proteínas G/agonistas , Receptores Acoplados a Proteínas G/metabolismoRESUMO
BACKGROUND: Lung adenocarcinoma metastasizing to the brain results in a notable increase in patient mortality. The high incidence and its impact on survival presents a critical unmet need to develop an improved understanding of its mechanisms. METHODS: To identify genes that drive brain metastasis of tumor cells, we collected cerebrospinal fluid samples and paired plasma samples from 114 lung adenocarcinoma patients with brain metastasis and performed 168 panel-targeted gene sequencing. We examined the biological behavior of PMS2 (PMS1 Homolog 2)-amplified lung cancer cell lines through wound healing assays and migration assays. In vivo imaging techniques are used to detect fluorescent signals that colonize the mouse brain. RNA sequencing was used to compare differentially expressed genes between PMS2 amplification and wild-type lung cancer cell lines. RESULTS: We discovered that PMS2 amplification was a plausible candidate driver of brain metastasis. Via in vivo and in vitro assays, we validated that PMS2 amplified PC-9 and LLC lung cancer cells had strong migration and invasion capabilities. The functional pathway of PMS2 amplification of lung cancer cells is mainly enriched in thiamine, butanoate, glutathione metabolism. CONCLUSION: Tumor cells elevated expression of PMS2 possess the capacity to augment the metastatic potential of lung cancer and establish colonies within the brain through metabolism pathways.
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This study systematically reviewed the application of large language models (LLMs) in medicine, analyzing 550 selected studies from a vast literature search. LLMs like ChatGPT transformed healthcare by enhancing diagnostics, medical writing, education, and project management. They assisted in drafting medical documents, creating training simulations, and streamlining research processes. Despite their growing utility in assisted diagnosis and improving doctor-patient communication, challenges persisted, including limitations in contextual understanding and the risk of over-reliance. The surge in LLM-related research indicated a focus on medical writing, diagnostics, and patient communication, but highlighted the need for careful integration, considering validation, ethical concerns, and the balance with traditional medical practice. Future research directions suggested a focus on multimodal LLMs, deeper algorithmic understanding, and ensuring responsible, effective use in healthcare.
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BACKGROUND: The burgeoning demand for hepatectomy in elderly patients with hepatocellular carcinoma (HCC) necessitates improved perioperative care. Geriatric populations frequently experience functional decline and frailty, predisposing them to adverse postoperative outcomes. The Barthel Index serves as a reliable measure for assessing functional capacity, and this study evaluates its impact on surgical textbook outcomes (TOs) in elderly HCC patients. METHODS: A multicenter retrospective cohort study analyzed elderly patients (≥70 years) following hepatectomy for HCC between 2013 and 2021. Utilizing a Barthel Index cut-off value of 85, patients were divided into two groups: with and without preoperative functional decline and frailty. The primary outcome was the rate of TO, encompassing seven criteria. TO rates were compared between groups, and multivariate logistic regression analyses identified independent risks for achieving TOs. RESULTS: Of 497 elderly patients, 157 (31.6 â%) exhibited preoperative functional decline and frailty (Barthel Index score <85). The overall TO rate was 58.6 â%. Patients with preoperative Barthel Index score <85 had significantly lower TO rates compared to patients with score ≥85 (29.3 â% vs. 72.1 â%, P â< â0.001). Multivariate analysis revealed preoperative Barthel Index score <85 as an independent risk for achieving TO (odds ratio 3.413, 95 â% confidence interval 1.879-6.198, P â< â0.001). Comparable results were observed in the subgroups of patients undergoing open and laparoscopic hepatectomy. CONCLUSION: Preoperative Barthel Index-based assessment of functional decline and frailty significantly predicts TOs following hepatectomy in elderly HCC patients, enabling identification of high-risk patients and informing preoperative management and postoperative care within geriatric oncology.