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BACKGROUND: Endoscopic retrograde cholangiopancreatography (ERCP) has become a routine endoscopic procedure that is essential for diagnosing and managing various conditions, including gallstone extraction and the treatment of bile duct and pancreatic tumors. Despite its efficacy, post-ERCP infections - particularly those caused by carbapenem-resistant Enterobacterales (CRE) - present significant risks. These risks highlight the need for accurate predictive models to enhance postprocedural care, reduce the mortality risk associated with post-ERCP CRE sepsis, and improve patient outcomes in the context of increasing antibiotic resistance. OBJECTIVE: This study aimed to examine the risk factors for 30-day mortality in patients with CRE sepsis following ERCP and to develop a nomogram for accurately predicting 30-day mortality risk. METHODS: Data from 195 patients who experienced post-ERCP CRE sepsis between January 2010 and December 2022 were analyzed. Variable selection was optimized via the least absolute shrinkage and selection operator (LASSO) regression model. Multivariate logistic regression analysis was then employed to develop a predictive model, which was evaluated in terms of discrimination, calibration, and clinical utility. Internal validation was achieved through bootstrapping. RESULTS: The nomogram included the following predictors: age > 80 years (hazard ratio [HR] 2.61), intensive care unit (ICU) admission within 90 days prior to ERCP (HR 2.64), hypoproteinemia (HR 4.55), quick Pitt bacteremia score ≥ 2 (HR 2.61), post-ERCP pancreatitis (HR 2.52), inappropriate empirical therapy (HR 3.48), delayed definitive therapy (HR 2.64), and short treatment duration (< 10 days) (HR 5.03). The model demonstrated strong discrimination and calibration. CONCLUSIONS: This study identified significant risk factors associated with 30-day mortality in patients with post-ERCP CRE sepsis and developed a nomogram to accurately predict this risk. This tool enables healthcare practitioners to provide personalized risk assessments and promptly administer appropriate therapies against CRE, thereby reducing mortality rates.
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Colangiopancreatografia Retrógrada Endoscópica , Infecciones por Enterobacteriaceae , Nomogramas , Sepsis , Humanos , Colangiopancreatografia Retrógrada Endoscópica/efectos adversos , Masculino , Femenino , Estudios Retrospectivos , Factores de Riesgo , Anciano , Persona de Mediana Edad , Sepsis/mortalidad , Sepsis/microbiología , Infecciones por Enterobacteriaceae/mortalidad , Infecciones por Enterobacteriaceae/tratamiento farmacológico , Enterobacteriaceae Resistentes a los Carbapenémicos/aislamiento & purificación , Antibacterianos/uso terapéutico , Antibacterianos/farmacología , Anciano de 80 o más AñosRESUMEN
Acute pancreatitis (AP) is an inflammatory disease characterized by localized pancreatic injury and a systemic inflammatory response. Fatty acids (FAs), produced during the breakdown of triglycerides (TGs) in blood and peripancreatic fat, escalate local pancreatic inflammation to a systemic level by damaging pancreatic acinar cells (PACs) and triggering M1 macrophage polarization. This paper provides a comprehensive analysis of lipases' roles in the onset and progression of AP, as well as the effects of long-chain fatty acids (LCFAs) on the function of pancreatic acinar cells (PACs). Abnormalities in the function of PACs include Ca2+ overload, premature trypsinogen activation, protein kinase C (PKC) expression, endoplasmic reticulum (ER) stress, and mitochondrial and autophagic dysfunction. The study highlights the contribution of long-chain saturated fatty acids (LC-SFAs), especially palmitic acid (PA), to M1 macrophage polarization through the activation of the NLRP3 inflammasome and the NF-κB pathway. Furthermore, we investigated lipid lowering therapy for AP. This review establishes a theoretical foundation for pro-inflammatory mechanisms associated with FAs in AP and facilitating drug development.
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Intracranial aneurysms (IAs), as a common cerebrovascular disease, claims a worldwide morbidity rate of 3.2%. Inflammation, pivotal in the pathogenesis of IAs, influences their formation, growth, and rupture. This review investigates aspirin's modulation of inflammatory pathways within this context. With IAs carrying significant morbidity and mortality upon IAs rupture and current interventions limited to surgical clipping and endovascular coiling, the quest for pharmacological options is imperative. Aspirin's role in cardiovascular prevention, due to its anti-inflammatory effects, presents a potential therapeutic avenue for IAs. In this review, we examine aspirin's efficacy in experimental models and clinical settings, highlighting its impact on the progression and rupture risks of unruptured IAs. The underlying mechanisms of aspirin's impact on IAs are explored, with its ability examined to attenuate endothelial dysfunction and vascular injury. This review may provide a theoretical basis for the use of aspirin, suggesting a promising strategy for IAs management. However, the optimal dosing, safety, and long-term efficacy remain to be established. The implications of aspirin therapy are significant in light of current surgical and endovascular treatments. Further research is encouraged to refine aspirin's clinical application in the management of unruptured IAs, with the ultimate aim of reducing the incidence of aneurysms rupture.
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OBJECTIVE: The aim of this network meta-analysis was to compare the improvement effects of various exercise interventions and mindfulness-based interventions to determine the best interventions for the improvement of cognitive impairment. DESIGN: 7 databases were searched to screen RCTs of exercise interventions and mindfulness-based interventions to improve cognitive impairment. The network meta-analysis was performed using Revman 5.3, R 4.2.1 and ADDIS 1.16.8 software. RESULTS: 34 RCTs involving 14 interventions were included in the study. In terms of cognitive function, except for mindfulness-based stress reduction, all interventions showed significantly greater improvement in cognitive function compared with conventional therapy. Physical activity and Qigong showed better effect in improving executive function. In terms of improving verbal memory, compensatory cognitive training, neurofeedback training, Qigong and sham Qigong were more effective than other interventions. On performing surface under the cumulative ranking curve analysis, acceptance and commitment therapy, neurofeedback training, Qigong, and mediation had the best effects on cognitive function, quality of life, executive function, and processing speed, respectively. CONCLUSIONS: Mindfulness-based interventions were found to be more effective than exercise interventions for alleviating cognitive impairment. More robust RCTs focusing on acceptance and commitment therapy for cognitive impairment are required to support the current evidence.
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Homograft rejection is the main cause of heart transplantation failure. The role of TLR2, a major member of the toll-like receptor (TLR) family, in transplantation rejection is has yet to be elucidated. In this study, we used a mouse model of acute cardiac transplantation rejection to investigate whether the TLR2 signalling pathway can regulate cardiac transplantation rejection by regulating alloreactive IL-17+γδT (γδT17) cells. We found that the expression of TLR2 on the surface of dendritic cells (DCs) and macrophages increased during acute transplantation rejection. In addition, our investigation revealed that γδT17 cells exert a significant influence on acute cardiac transplantation rejection. TLR2 gene knockout resulted in an increase in alloreactive γδT17 cells in the spleen and heart grafts of recipient mice compared with wild-type recipient mice and an increase in the mRNA expression of IL-17, IL-1ß, CCR6, and CCL20 in the heart grafts. In an in vitro experiment, a mixed lymphocyte reaction was conducted to assess the impact of TLR2 deficiency on the generation of γδT17 cells, which further substantiated a significant increase compared to that in wild-type controls. Furthermore, the mixed lymphocyte reaction showed that TLR2 regulated the production of γδT17 cells by regulating the ability of DCs to secrete IL-1ß. These results suggest that TLR2 signalling is important for regulating the generation of γδT17 cells after cardiac allograft transplantation.
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Trasplante de Corazón , Linfocitos Intraepiteliales , Receptor Toll-Like 2 , Animales , Ratones , Rechazo de Injerto , Interleucina-17/genética , Interleucina-17/metabolismo , Ratones Endogámicos C57BL , Ratones Noqueados , Receptor Toll-Like 2/genética , Receptor Toll-Like 2/metabolismo , Trasplante Homólogo , Linfocitos Intraepiteliales/inmunologíaRESUMEN
Shank3, a key molecule related to the development and deterioration of autism, has recently been found to downregulate in the murine brain after ischemia/reperfusion (I/R). Despite this discovery, however, its effects on neuronal injury and the mechanism underlying the effects remain to be clarified. To address this, in this study, based on genetically modified mice models, we revealed that the expression of Shank3 showed a time-dependent change in murine hippocampal neurons after I/R, and that conditional knockout (cko) of Shank3 in neurons resulted in aggravated neuronal injuries. The protective effects of Shank3 against oxidative stress and inflammation after I/R were achieved through direct binding STIM1 and subsequent proteasome-mediated degradation of STIM1. The STIM1 downregulation induced the phosphorylation of downstream Nrf2 Ser40, which subsequently translocated to the nucleus, and further increased the expression of antioxidant genes such as NQO1 and HO-1 in HT22 cells. In vivo, the study has further confirmed that double knockout of Shank3 and Stim1 alleviated oxidative stress and inflammation after I/R in Shank3cko mice. In conclusion, the present study has demonstrated that Shank3 interacts with STIM1 and inhibits post-I/R neuronal oxidative stress and inflammatory response via the Nrf2 pathway. This interaction can potentially contribute to the development of a promising method for I/R treatment.
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Isquemia Encefálica , Daño por Reperfusión , Ratones , Animales , Factor 2 Relacionado con NF-E2/genética , Factor 2 Relacionado con NF-E2/metabolismo , Daño por Reperfusión/genética , Daño por Reperfusión/metabolismo , Estrés Oxidativo , Isquemia Encefálica/genética , Isquemia Encefálica/metabolismo , Inflamación/genética , Inflamación/metabolismo , Reperfusión , Neuronas/metabolismo , Apoptosis , Proteínas de Microfilamentos/metabolismo , Proteínas de Microfilamentos/farmacología , Proteínas del Tejido Nervioso/genética , Proteínas del Tejido Nervioso/metabolismoRESUMEN
Acute hypobaric hypoxic brain damage is a potentially fatal high-altitude sickness. Autophagy plays a critical role in ischemic brain injury, but its role in hypobaric hypoxia (HH) remains unknown. Here we used an HH chamber to demonstrate that acute HH exposure impairs autophagic activity in both the early and late stages of the mouse brain, and is partially responsible for HH-induced oxidative stress, neuronal loss, and brain damage. The autophagic agonist rapamycin only promotes the initiation of autophagy. By proteome analysis, a screen showed that protein dynamin2 (DNM2) potentially regulates autophagic flux. Overexpression of DNM2 significantly increased the formation of autolysosomes, thus maintaining autophagic flux in combination with rapamycin. Furthermore, the enhancement of autophagic activity attenuated oxidative stress and neurological deficits after HH exposure. These results contribute to evidence supporting the conclusion that DNM2-mediated autophagic flux represents a new therapeutic target in HH-induced brain damage.
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Hipoxia , Estrés Oxidativo , Ratones , Animales , Autofagia , Cognición , Sirolimus/uso terapéuticoRESUMEN
This study presents a novel method for the regioselective coupling of gem-difluorinated cyclopropanes with gem-diborylmethane, utilizing a Pd-catalyst system. This innovative approach enables the synthesis of 2-fluoroalkenyl monoboronate scaffolds with high Z-selectivity. The resulting products undergo further transformations, including oxidation, Suzuki cross-coupling, and trifluoroborylation, all of which are achieved with good yields. This work introduces a valuable synthetic pathway to access important fluorinated compounds for various applications in organic chemistry.
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Pancreatic ductal adenocarcinoma (PDAC) remains one of the most devastating diseases; it has a considerably poor prognosis and may become the second most lethal malignancy in the next 10 years. Chemotherapeutic resistance is common in PDAC; thus, it is necessary to exploit effective alternative drugs. In recent years, traditional folk medicines and their extracts have shown great potential in cancer treatment. The seed of Lagenaria siceraria (Molina) Standl. is a traditional medicine in Asia. Because of its analgesic effects and ability to reduce swelling, it is often used as an adjuvant treatment for abdominal tumors. Cucurbitacin compounds are extracts abundant in Lagenaria siceraria (Molina) Standl. Here, we found that cucurbitacin C (CuC), a member of the cucurbitacin family, has apparent anti-PDAC therapeutic properties. CuC decreased the viability and suppressed the proliferation of PDAC cells in a time- and dose-dependent manner. Further studies revealed that CuC inhibited cell migration and invasion by inhibiting epithelial-mesenchymal transition (EMT). In addition, G2/M arrest was induced, and the apoptotic pathway was activated. Transcriptomic and bioinformatic analyses showed that CuC inhibited the cGMP-PKG-VASP axis, increasing the content of cGMP to restore tumor characteristics. The antitumor activity of CuC in vivo was verified through animal experiments, and no obvious side effects were observed. Overall, our study indicates a candidate therapeutic compound for PDAC that is worthy of further development.
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Carcinoma Ductal Pancreático , Neoplasias Pancreáticas , Animales , Apoptosis , Cucurbitacinas/farmacología , Línea Celular Tumoral , Proliferación Celular , Puntos de Control de la Fase G2 del Ciclo Celular , Carcinoma Ductal Pancreático/metabolismo , Neoplasias Pancreáticas/metabolismo , Movimiento Celular , Regulación Neoplásica de la Expresión Génica , Transición Epitelial-Mesenquimal , Neoplasias PancreáticasRESUMEN
Escherichia coli O157:H7 can recover from sublethally injured (SI) state, which causes threat of foodborne illness. Adhesion plays a key role in the carriage of pathogens in food. In this study, we investigated the adhesion ability of SI and recovered E. coli O157:H7 wildtype and its three pili-deficient mutants (curli, type 1 fimbriae, and type IV pili) on six food-related surfaces. Plate counting was used to determine adhesion population after washing and oscillating the surfaces. Spinach exhibited the stronger adhesion population of E. coli O157:H7 than the other fresh produces (p < 0.05). In addition, at least one key pili dominated adhesion on these surfaces, and curli was always included. The adhesion population and contribution of different types of pili were jointly affected by surface and physiological state. This can be attributed to high hydrophobicity and positive charge density on surface and different expression levels of csgB, fimA, fimC and ppdD in SI and recovered cells. Among glucose, mannose, maltose, fructose, lactose, and sucrose, addition of 0.5% mannose could reduce adhesion of cells at all physiological states on stainless steel. Overall, this research will provide support for controlling adhesion of SI and recovered E. coli O157:H7.
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Escherichia coli O157 , Escherichia coli O157/metabolismo , Adhesión Bacteriana , Manosa/metabolismo , Recuento de Colonia Microbiana , Propiedades de Superficie , Microbiología de AlimentosRESUMEN
BACKGROUND: Observational studies have indicated that the incidence of primary biliary cholangitis (PBC) is higher in inflammatory bowel disease (IBD) patients than that in healthy people. However, whether the correlation is causal remains unclear. METHODS: The genetic associations with IBD were obtained from publicly available genome-wide association studies (GWAS) of European ancestry with 31 665 cases and 33 977 controls, consisting of 17 897 Crohn's disease (CD) and 13 768 ulcerative colitis (UC) cases. The genetic associations with PBC were obtained from a European GWAS with 2764 cases and 10 475 controls. A bidirectional two-sample Mendelian randomization (MR) design was implemented to determine the causal relationship between IBD and PBC. In the forward MR, the IBD was treated as the exposure while the PBC was the exposure in the reverse MR. The inverse-variance-weighted (IVW) method was utilized as the main statistic method, and a series of sensitivity analyses were performed to detect heterogeneity and horizontal pleiotropy. RESULTS: A total of 99 valid instrumental variables (IVs) were selected for IBD and the number of IVs for PBC was 18. The forward MR analysis indicated that genetically predicted IBD (UC and CD) was significantly associated with an increased risk of PBC (IVW OR = 1.343; 95% CI: 1.220-1.466). Similar casual associations were observed in UC (IVW OR = 1.244; 95% CI: 1.057-1.430) and CD (IVW OR = 1.269; 95% CI: 1.159-1.379). Such results were still consistent in multiple MR methods. The reverse MR analysis implicated that genetic susceptibility to PBC might not alter the risk of IBD (IVW OR = 1.070; 95% CI: 0.984-1.164). CONCLUSION: Our study found that genetically predicted IBD can increase the risk of PBC while not vice versa in the European population, which may enlighten the aetiology of PBC, together with the IBD patient management.
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Colitis Ulcerosa , Enfermedades Inflamatorias del Intestino , Cirrosis Hepática Biliar , Humanos , Estudio de Asociación del Genoma Completo , Cirrosis Hepática Biliar/genética , Análisis de la Aleatorización Mendeliana , Colitis Ulcerosa/genéticaRESUMEN
The early aseptic immune response is the key factor leading to the aggravation of acute pancreatitis (AP). Toll-like receptor (TLR) 2 is an important member of the TLR family, but the role of TLR2 in AP remains to be investigated. In the present study, we found that TLR2 expression was significantly increased in AP patients. In a mouse model of cerulein-induced AP, TLR2 deficiency resulted in reduced inflammation, reduced infiltration of pancreatic neutrophils and macrophages, and decreased expression of proinflammatory cytokines such as interleukin (IL)-1ß, IL-6, IL-17 and IL-18. In addition, transcriptomic analysis revealed that nod-like receptor family pyrin domain-containing 3 (NLRP3) expression was increased in AP, and there was a significant correlation between NLRP3 and TLR2. This study found that TLR2 deficiency can lead to a decrease in the activation of the NF-κB/NLRP3 signalling pathway, and the NLRP3 inhibitor MCC950 can alleviate AP in mice. Therefore, this study confirmed that TLR2 participates in the development of AP by activating the NF-κB/NLRP3 pathway. This study suggested that TLR2 might be a novel therapeutic target for AP.
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FN-kappa B , Pancreatitis , Animales , Humanos , Ratones , Enfermedad Aguda , Inflamasomas/metabolismo , FN-kappa B/metabolismo , Proteína con Dominio Pirina 3 de la Familia NLR/genética , Proteína con Dominio Pirina 3 de la Familia NLR/metabolismo , Pancreatitis/inducido químicamente , Pancreatitis/metabolismo , Receptor Toll-Like 2/genética , Receptor Toll-Like 2/metabolismoRESUMEN
Direct and selective fluoroarylations of nucleophilic secondary alkylanilines with polyfluoroarenes were first realized through visible-light-induced C-H/C-F couplings with the assistance of bases. Varieties of α-polyfluoroarylanilines were selectively produced with this protocol from polyfluoroarenes and N-alkylanilines, including natural products and pharmaceutical molecule derivatives. Mechanistic studies illustrated base-promoted photochemical C-H cleavage of the α-C-H bonds of alkylanilines to produce the N-α-carbon radical and then radical addition to polyfluoroarenes.
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Compuestos de Anilina , Luz , Compuestos de Anilina/química , Catálisis , Estructura Molecular , Carbono/químicaRESUMEN
AIM: To examine how the effects of hardiness, self-efficacy and positive academic emotion related to the SRL ability of undergraduate nursing students. DESIGN: A cross-sectional survey was designed. METHODS: A total of 395 Chinese undergraduate nursing students from two undergraduate colleges filled out the questionnaires from May to June 2019. The relationships between hardiness, self-efficacy, positive academic emotion and SRL ability were analysed by structural equation modelling. RESULTS: The response rate was 94.05%. SRL ability was significantly positive correlated with hardiness, self-efficacy and positive academic emotion in undergraduate nursing students. Self-efficacy (ß = 0.417, p < 0.001) and positive academic emotion (ß = 0.232, p < 0.001) showed a direct effect on the SRL ability. Although hardiness showed no direct effect on the SRL ability, it affected SRL ability through three indirect ways: self-efficacy (77.778%), positive academic emotion (14.184%) and the chain mediating effect from self-efficacy to positive academic emotion (8.038%). CONCLUSIONS: Nursing students with a higher level of hardiness would have higher self-efficacy, and more positive and stable academic emotions to obtain the better SRL ability. The produced model provides insights into several factors associated with SRL ability of nursing students. Hardiness, self-efficacy and positive academic emotion should be emphasized in the education of nursing students because these factors could improve their SRL ability and promote their life-long learning.
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Bachillerato en Enfermería , Estudiantes de Enfermería , Humanos , Estudiantes de Enfermería/psicología , Estudios Transversales , Análisis de Clases Latentes , AprendizajeRESUMEN
BACKGROUND: With the number of critically ill patients increasing in gastroenterology departments (GEDs), infections associated with Carbapenem-resistant Gram-negative bacteria (CR-GNB) are of great concern in GED. However, no CR-GNB bloodstream infection (BSI) risk prediction model has been established for GED patients. Almost universally, CR-GNB colonization precedes or occurs concurrently with CR-GNB BSI. The objective of this study was to develop a nomogram that could predict the risk of acquiring secondary CR-GNB BSI in GED patients who are carriers of CR-GNB. METHODS: We conducted a single-center retrospective case-control study from January 2020 to March 2022. Univariate and multivariable logistic regression analysis was used to identify independent risk factors of secondary CR-GNB bloodstream infections among CR-GNB carriers in the gastroenterology department. A nomogram was constructed according to a multivariable regression model. Various aspects of the established predicting nomogram were evaluated, including discrimination, calibration, and clinical utility. We assessed internal validation using bootstrapping. RESULTS: The prediction nomogram includes the following predictors: high ECOG PS, severe acute pancreatitis, diabetes mellitus, neutropenia, a long stay in hospital, and parenteral nutrition. The model demonstrated good discrimination and good calibration. CONCLUSIONS: With an estimate of individual risk using the nomogram developed in this study, clinicians and nurses can identify patients with a high risk of secondary CR-GNB BSI early.
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Intracerebral hemorrhage (ICH) is a devastating stroke type with high mortality and disability. Inflammatory response induced by macrophages/microglia (M/Ms) activation is one of the leading causes of brain damage after ICH. The anti-inflammatory effects of resveratrol (RSV) have already been evaluated in several models of central nervous system disease. Therefore, we designed the current study to assess the role of RSV in ICH and explore its downstream mechanism related to Sirt3. The autologous artery blood injection was administrated to create an ICH mouse model. M/Ms-specific Sirt3 knockout Sirt3f/f; CX3CR1-Cre (Sirt3 cKO) mouse was used to evaluate the role of Sirt3 on RSV treatment. Neuronal function and hematoma volume were assessed to indicate brain damage. The pro-inflammatory marker (CD16) and cytokine (TNF) were measured to evaluate the inflammatory effects. Our results showed that RSV treatment alleviates neurological deficits, reduces cell death, and increases hematoma clearance on day 7 after ICH. In addition, RSV effectively suppressed CD16+ M/Ms activation and decreased TNF release. In Sirt3 cKO mice, the protective effects of RSV were abolished, indicating the potential mechanism of RSV was partially due to Sirt3 signaling activation. Therefore, RSV could be a promising candidate and therapeutic agent for ICH and Sirt3 could be a potential target to inhibit inflammation.
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Lesiones Encefálicas , Sirtuina 3 , Ratones , Animales , Microglía/metabolismo , Resveratrol/farmacología , Resveratrol/uso terapéutico , Hemorragia Cerebral/complicaciones , Hemorragia Cerebral/tratamiento farmacológico , Hemorragia Cerebral/metabolismo , Macrófagos , Lesiones Encefálicas/metabolismo , Antiinflamatorios/farmacología , Antiinflamatorios/uso terapéutico , Antiinflamatorios/metabolismo , HematomaRESUMEN
The pathophysiological process of neuronal injury due to cerebral ischemia is complex among which disturbance of calcium homeostasis and autophagy are two major pathogenesis. However, it remains ambiguous whether the two factors are independent. Stromal interaction molecule 1 (STIM1) is the most important Ca2+ sensor mediating the store-operated Ca2+ entry (SOCE) through interacting with Orai1 and has recently been proven to participate in autophagy in multiple cells. In this study, we aimed to investigate the potential role of STIM1-induced SOCE on autophagy and whether its regulator function contributes to neuronal injury under hypoxic conditions using in vivo transient middle cerebral artery occlusion (tMCAO) model and in vitro oxygen and glucose deprivation (OGD) primary cultured neuron model respectively. The present data indicated that STIM1 induces autophagic flux impairment in neurons through promoting SOCE and inhibiting AKT/mTOR signaling pathway. Pharmacological inhibition of SOCE or downregulation of STIM1 with siRNA suppressed the autophagic activity in neurons. Moreover, stim1 knockdown attenuated neurological deficits and brain damage after tMCAO, which could be reversed by AKT/mTOR pathway inhibitor AZD5363. Together, the modulation of STIM1 on autophagic activation indicated the potential link between Ca2+ homeostasis and autophagy which provided evidence that STIM1 could be a promising therapeutic target for ischemic stroke.
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Calcio , Accidente Cerebrovascular Isquémico , Autofagia , Calcio/metabolismo , Señalización del Calcio/fisiología , Hipocampo/metabolismo , Neuronas/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , Molécula de Interacción Estromal 1/genética , Molécula de Interacción Estromal 1/metabolismo , Serina-Treonina Quinasas TOR/metabolismo , AnimalesRESUMEN
Computerized tomography (CT) is of great significance for the localization and diagnosis of liver cancer. Many scholars have recently applied deep learning methods to segment CT images of liver and liver tumors. Unlike natural images, medical image segmentation is usually more challenging due to its nature. Aiming at the problem of blurry boundaries and complex gradients of liver tumor images, a deep supervision network based on the combination of high-efficiency channel attention and Res-UNet++ (ECA residual UNet++) is proposed for liver CT image segmentation, enabling fully automated end-to-end segmentation of the network. In this paper, the UNet++ structure is selected as the baseline. The residual block feature encoder based on context awareness enhances the feature extraction ability and solves the problem of deep network degradation. The introduction of an efficient attention module combines the depth of the feature map with spatial information to alleviate the uneven sample distribution impact; Use DiceLoss to replace the cross-entropy loss function to optimize network parameters. The liver and liver tumor segmentation accuracy on the LITS dataset was 95.8% and 89.3%, respectively. The results show that compared with other algorithms, the method proposed in this paper achieves a good segmentation performance, which has specific reference significance for computer-assisted diagnosis and treatment to attain fine segmentation of liver and liver tumors.
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Neoplasias Hepáticas , Humanos , Neoplasias Hepáticas/diagnóstico por imagen , Algoritmos , Diagnóstico por Computador , Tomografía Computarizada por Rayos X , Procesamiento de Imagen Asistido por ComputadorRESUMEN
Intensification of urban construction has gradually destroyed human habitat ecosystems. Plants, which serve as the foundation of ecosystems, require green, low-cost, and effective technologies to sustain their growth in stressful environments. A total of 286 keywords and 10 clusters from the bibliometric analysis of 529 articles (1999-2023) indicate the increasing importance of research on microbial functionality in landscape ecosystems. Phosphate solubilizing microorganisms (PSMs) also improve plant disease resistance, adaptability, and survival. PSMs are widely used to promote plant growth and improve ecological quality. They can increase the availability of phosphorus in the soil and reduce the dependence of plants on chemical fertilizers. Microorganisms regulate phosphorus as key tools in landscape ecosystems. Most importantly, in urban and rural landscape practices, PSMs can be applied to green spaces, residential landscapes, road greening, and nursery planting, which play significant roles in improving vegetation coverage, enhancing plant resistance, improving environmental quality, and mitigating the heat island effect. PSMs are also helpful in restoring the ecological environment and biodiversity of polluted areas, such as brownfields, to provide residents with a more liveable living environment. Therefore, the multiple efficacies of PSM are expected to play increasingly important roles in the construction of urban and rural landscape ecosystems.
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BACKGROUND: A key outcome in coronary heart disease (CHD) is Health Related Quality of Life (HRQoL), and family functioning is important in the management of CHD. But few studies have examined both together, and little is known about them among inpatients with CHD in less developed areas of China. Therefore, this study aimed to assess the HRQoL and family functioning status of inpatients with CHD in Lanzhou from Northwest China, and identify the factors that affect their HRQoL. METHODS: A crosssectional study was conducted in 224 CHD inpatients at one major hospital. Sociodemographic data and disease information of CHD inpatients were collected by face-to-face using a structured questionnaire and data were also obtained from patient medical records. HRQoL was measured using the Sickness Impact Profile (SIP). Family functioning was measured using the family APGAR index. Multiple binary logistic regression analysis (MBLRA) was used to explore potential risk factors associated with HRQoL, and Pearson's correlations were used to assess the relationship between family functioning and HRQoL. RESULTS: The overall, physical and psychosocial SIP scores were 25.03 ± 8.52, 18.61 ± 9.90 and 28.08 ± 9.64, respectively. The total family APGAR score was 6.11 ± 2.45. MBLRA found older age, poorer cardiac function and more severe disease were associated with poorer HRQoL, while better family functioning, higher monthly income, and urban living were associated with better HRQoL. Family functioning was weakly to moderately correlated with total and psychosocial HRQoL. CONCLUSIONS: Older and less affluent inpatients with lower educational level, less family support and more severe CHD have poorest quality of life, and health care providers should consider interventions to support them.