ABSTRACT
AIMS: To systematically evaluate and analyse literature concerning the factors influencing the implementation of clinical practice guidelines related to enteral nutrition in the adult intensive care unit. BACKGROUND: Guidelines serve as crucial tools for guiding clinical practice. However, a significant gap persists between current clinical practice and guidelines pertaining to enteral nutrition. It is essential to identify the reasons behind this disparity to foster clinical transformation. METHODS: A mixed-methods systematic review. DATA SOURCES: A systematic search was conducted across PubMed, Embase, Medline, Cochrane, PsycINFO and CNKI databases to identify impediments and facilitators to the implementation of ICU clinical practice guidelines related to enteral nutrition. The types of studies included quantitative, qualitative and mixed-methods studies. The search spanned from January 2003 to January 2024 and was updated in May 2024. The quality assessment of the included literature was conducted using the Mixed-Methods Study Evaluation Tool (MMAT). Data analysis was performed using a data-based convergent integration approach. The protocol for this study was prospectively registered (PROSPERO2023, CRD42023483287). RESULTS: Twenty papers were finally included, and 65 findings were extracted, integrating a total of three categories, Category 1: healthcare provider factors, including three sub-themes: knowledge of guideline-related knowledge and awareness of guideline application; social/professional roles and identity domains; beliefs, attitudes and self-efficacy; collaboration, Category 2: practice environments, including two sub-themes: environmental factors and resource areas; systems and behavioural norms, Category 3: patient values and nutritional support preferences including two sub-themes: patient disease status and value orientation. CONCLUSION: Healthcare professionals should analyse obstacles and facilitators to guideline implementation from multiple perspectives, strengthen healthcare collaboration, improve education and training systems, correct misperceptions and increase awareness of evidence-based practice.
ABSTRACT
Amyloid-ß (Aß) is thought to be neuronally derived in Alzheimer's disease (AD). However, transcripts of amyloid precursor protein (APP) and amyloidogenic enzymes are equally abundant in oligodendrocytes (OLs). By cell-type-specific deletion of Bace1 in a humanized knock-in AD model, APPNLGF, we demonstrate that OLs and neurons contribute to Aß plaque burden. For rapid plaque seeding, excitatory projection neurons must provide a threshold level of Aß. Ultimately, our findings are relevant for AD prevention and therapeutic strategies.
ABSTRACT
Siderophores are small molecule iron chelators. The entomopathogenic fungus Beauveria bassiana produces a plethora of siderophores under iron-limiting conditions. In this study, a siderophore biosynthesis pathway, akin to the general pathway observed in filamentous fungi, was revealed in B. bassiana. Among the siderophore biosynthesis genes (SID), BbSidA was required for the production of most siderophores, and the SidC and SidD biosynthesis gene clusters were indispensable for the production of ferricrocin and fusarinine C, respectively. Biosynthesis genes play various roles in siderophore production, vegetative growth, stress resistance, development, and virulence, in which BbSidA plays the most important role. Accordingly, B. bassiana employs a cocktail of siderophores for iron metabolism, which is essential for fungal physiology and host interactions. This study provides the initial network for the genetic modification of siderophore biosynthesis, which not only aims to improve the efficacy of biocontrol agents but also ensures the efficient production of siderophores.
Subject(s)
Beauveria , Biosynthetic Pathways , Fungal Proteins , Siderophores , Beauveria/metabolism , Beauveria/genetics , Siderophores/metabolism , Siderophores/biosynthesis , Fungal Proteins/genetics , Fungal Proteins/metabolism , Iron/metabolism , Animals , Insecta/microbiology , Multigene Family , Ferrichrome/analogs & derivativesABSTRACT
[This corrects the article DOI: 10.3389/fphar.2017.00476.].
ABSTRACT
Mitochondrial DNA (mtDNA) is pivotal for mitochondrial morphology and function. Upon mtDNA damage, mitochondria undergo quality control mechanisms, including fusion, fission, and mitophagy. Real-time monitoring of mtDNA enables a deeper understanding of its effect on mitochondrial function and morphology. Controllable induction and real-time tracking of mtDNA dynamics and behavior are of paramount significance for studying mitochondrial function and morphology, facilitating a deeper understanding of mitochondria-related diseases. In this work, a fluorescent platinum complex was designed and developed that not only induces mitochondrial DNA (mtDNA) aggregation but also triggers mitochondrial autophagy (mitophagy) through the MDV pathway for damaged mtDNA clearance in living cells. Additionally, this complex allows for the real-time monitoring of these processes. This complex may serve as a valuable tool for studying mitochondrial microautophagy and holds promise for broader applications in cellular imaging and disease research.
Subject(s)
DNA, Mitochondrial , Fluorescent Dyes , Mitophagy , DNA, Mitochondrial/metabolism , Humans , Fluorescent Dyes/chemistry , Mitochondria/metabolism , Platinum/chemistry , HeLa CellsABSTRACT
17ß-E2 is used in animal growth regulation and agricultural fertilizer, and even ng L-1 mass concentration levels can show biological effects. In this work, Ag NPs was used as surface-enhanced Raman spectroscopy (SERS) source and WS2 was synthesized by a simple method to provide a uniform distribution platform for Ag NPs. The MIP was the shell, which can selectively enrich the target molecule, pull the distance between the target molecule and SERS source, and protect Ag NPs. A cyclable SERS substrate with high sensitivity for detecting 17ß-E2 in food was constructed. The optimized WS2/Ag@MIP as SERS substrate has the advantages of high Enhanced Factor (EF = 2.78 × 109), low detection limit (LOD = 0. 0958 pM), strong anti-interference ability, and good recycling performance. Moreover, the detection of 17ß-E2 in real samples still has good accuracy. This work provides a new possibility for the trace detection of 17ß-E2 in food.
ABSTRACT
Neonicotinoids (NEOs), the most widely used class of insecticides, are pervasive in the environment, eliciting concerns due to their hydrophilicity, persistence, and potential ecological risks. As the leading pesticide consumer, China shows significant regional disparities in NEO contamination. This review explores NEO distribution, sources, and toxic risks across China. The primary NEO pollutants identified in environmental samples include imidacloprid, thiamethoxam, and acetamiprid. In the north, corn cultivation represents the principal source of NEOs during wet seasons, while rice dominates in the south year-round. The high concentration levels of NEOs have been detected in the aquatic environment in the southern regions (130.25 ng/L), the urban river Sects. (157.66 ng/L), and the downstream sections of the Yangtze River (58.9 ng/L), indicating that climate conditions and urban pollution emissions are important drivers of water pollution. Neonicotinoids were detected at higher levels in agricultural soils compared to other soil types, with southern agricultural areas showing higher concentrations (average 27.21 ng/g) than northern regions (average 12.77 ng/g). Atmospheric NEO levels were lower, with the highest concentration at 1560 pg/m3. The levels of total neonicotinoid pesticides in aquatic environments across China predominantly exceed the chronic toxicity ecological threshold of 35 ng/L, particularly in the regions of Beijing and the Qilu Lake Basin, where they likely exceed the acute toxicity ecological threshold of 200 ng/L. In the future, efforts should focus on neonicotinoid distribution in agriculturally developed regions of Southwest China, while also emphasizing their usage in urban greening and household settings.
ABSTRACT
Background: Non-suicidal self-injury (NSSI) is a significant social issue, especially among adolescents with major depressive disorder (MDD). This study aimed to construct a risk prediction model using machine learning (ML) algorithms, such as XGBoost and random forest, to identify interventions for healthcare professionals working with adolescents with MDD. Methods: This study investigated 488 adolescents with MDD. Adolescents was randomly divided into 75% training set and 25% test set to testify the predictive value of risk prediction model. The prediction model was constructed using XGBoost and random forest algorithms. We evaluated the area under the receiver operating characteristic curve (AUC), sensitivity, specificity, accuracy, recall, F Score of the two models for comparing the performance of the two models. Results: There were 161 (33.00%) participants having NSSI. Compared without NSSI, there were statistically significant differences in gender (P=0.035), age (P=0.036), depressive symptoms (P=0.042), sleep quality (P=0.030), dysfunctional attitudes (P=0.048), childhood trauma (P=0.046), interpersonal problems (P=0.047), psychoticism (P) (P=0.049), neuroticism (N) (P=0.044), punishing and Severe (F2) (P=0.045) and Overly-intervening and Protecting (M2) (P=0.047) with NSSI. The AUC values for random forest and XGBoost were 0.780 and 0.807, respectively. The top five most important risk predictors identified by both machine learning methods were dysfunctional attitude, childhood trauma, depressive symptoms, F2 and M2. Conclusion: The study demonstrates the suitability of prediction models for predicting NSSI behavior in Chinese adolescents with MDD based on ML. This model improves the assessment of NSSI in adolescents with MDD by health care professionals working. This provides a foundation for focused prevention and interventions by health care professionals working with these adolescents.
ABSTRACT
The newly identified estrogen receptor, G protein-coupled receptor 30 (GPR30), is prevalent in the brain and has been shown to provide significant neuroprotection. Recent studies have linked ferroptosis, a newly characterized form of programmed cell death, closely with cerebral ischemia-reperfusion injury (CIRI), highlighting it as a major contributing factor. Consequently, our research aimed to explore the potential of GPR30 targeting in controlling neuronal ferroptosis and lessening CIRI impacts. Results indicated that GPR30 activation not only improved neurological outcomes and decreased infarct size in a mouse model but also lessened iron accumulation and malondialdehyde formation post-middle cerebral artery occlusion (MCAO). This protective effect extended to increased levels of Nrf2 and GPX4 proteins. Similar protective results were replicated in PC12 cells subjected to Oxygen Glucose Deprivation and Reoxygenation (OGD/R) using the GPR30-specific agonist G1. Importantly, inhibition of Nrf2 with ML385 curtailed the neuroprotective effects of GPR30 activation, suggesting that GPR30 mitigates CIRI primarily through inhibition of neuronal ferroptosis via upregulation of Nrf2 and GPX4.
Subject(s)
Ferroptosis , Infarction, Middle Cerebral Artery , Mice, Inbred C57BL , NF-E2-Related Factor 2 , Phospholipid Hydroperoxide Glutathione Peroxidase , Receptors, Estrogen , Receptors, G-Protein-Coupled , Reperfusion Injury , Signal Transduction , Animals , NF-E2-Related Factor 2/metabolism , Reperfusion Injury/prevention & control , Reperfusion Injury/metabolism , Receptors, G-Protein-Coupled/metabolism , Receptors, G-Protein-Coupled/genetics , Receptors, G-Protein-Coupled/physiology , Ferroptosis/drug effects , Ferroptosis/physiology , Signal Transduction/drug effects , Mice , PC12 Cells , Phospholipid Hydroperoxide Glutathione Peroxidase/genetics , Phospholipid Hydroperoxide Glutathione Peroxidase/metabolism , Rats , Male , Neuroprotective Agents/therapeutic use , Neuroprotective Agents/pharmacology , Disease Models, AnimalABSTRACT
BACKGROUND: Prior researches have highlighted inverse associations between levels of circulating very-long chain saturated fatty acids (VLCSFAs) and coronary heart disease (CHD). However, the intricate links involving VLCSFAs, gut microbiota, and bile acids remain underexplored. OBJECTIVE: This study examined the association of erythrocyte VLCSFAs with CHD incidence, focusing on the mediating role of gut microbiota and fecal bile acids. METHODS: This 10-year prospective study included 2383 participants without CHD at baseline. Erythrocyte VLCSFAs (arachidic acid [C20:0], behenic acid [C22:0], and lignoceric acid [C24:0]) were measured using gas chromatography at baseline and 274 CHD incidents were documented in triennial follow-ups. Gut microbiota in 1744 participants and fecal bile acid metabolites in 945 participants were analyzed using 16S rRNA sequencing and UPLC-MS/MS at middle-term. RESULTS: The multivariable-adjusted HRs (95%CI) for CHD incidence in highest vs. lowest quartiles were 0.87 (0.61, 1.25) for C20:0, 0.63 (0.42,0.96) for C22:0, 0.59 (0.41,0.85) for C24:0, and 0.57 (0.39, 0.83) for total VLCSFAs. Participants with higher total VLCSFA levels exhibited increased abundances of Holdemanella, Coriobacteriales Incertae Sedis spp., Ruminococcaceae UCG-005 and UCG-010, and Lachnospiraceae ND3007 group. These five genera generated microbial score (ODMS) that accounted for 11.52% of the total VLCSFAs-CHD association (Pmediation =0.018). Bile acids tauro_α_ and tauro_ß_muricholic acid (T_α_ and T_ß_MCA) were inversely associated with ODMS and positively associated with incident CHD. Opposite associations were found for glycolithocholic acid (GLCA), glycodeoxycholic acid (GDCA). Mediation analyses indicated that GLCA, GDCA, and T_α_ and T_ß_MCA explained 56.40%, 35.19%, and 26.17% of the ODMS-CHD association, respectively (Pmediation =0.002, 0.008, and 0.020). CONCLUSIONS: Elevated erythrocyte VLCSFAs are inversely associated with CHD risk in the Chinese population, with gut microbiota and fecal bile acid profiles potentially mediating this association. The identified microbiota and bile acid metabolites may serve as potential intervention targets in future studies. CLINICAL TRIAL REGISTRY NUMBER: NCT03179657.
ABSTRACT
Background: Sepsis triggers a strong inflammatory response, often leading to organ failure and high mortality. The role of serum albumin levels in sepsis is critical but not fully understood, particularly regarding the significance of albumin level changes over time. This study utilized Group-based Trajectory Modeling (GBTM) to investigate the patterns of serum albumin changes and their impact on sepsis outcomes. Methods: We conducted a retrospective analysis on ICU patients from West China Hospital (2015-2022), employing GBTM to study serum albumin fluctuations within the first week of ICU admission. The study factored in demographics, clinical parameters, and comorbidities, handling missing data through multiple imputation. Outcomes assessed included 28-day mortality, overall hospital mortality, and secondary complications such as AKI and the need for mechanical ventilation. Results: Data from 1,950 patients revealed four serum albumin trajectories, showing distinct patterns of consistently low, increasing, moderate, and consistently high levels. These groups differed significantly in mortality, with the consistently low level group experiencing the highest mortality. No significant difference in 28-day mortality was observed among the other groups. Subgroup analysis did not alter these findings. Conclusion: The study identified four albumin trajectory groups in sepsis patients, highlighting that those with persistently low levels had the worst outcomes, while those with increasing levels had the best. Stable high levels above 30 g/L did not change outcomes significantly. These findings can inform clinical decisions, helping to identify high-risk patients early and tailor treatment approaches.
ABSTRACT
Long noncoding RNA and microRNA are regulatory noncoding RNAs that are implicated in Alzheimer's disease, but the role of long noncoding RNA-associated competitive endogenous RNA has not been fully elucidated. The long noncoding RNA growth arrest-specific 5 (GAS5) is a member of the 5'-terminal oligopyrimidine gene family that may be involved in neurological disorders, but its role in Alzheimer's disease remains unclear. This study aimed to investigate the function of GAS5 and construct a GAS5-associated competitive endogenous RNA network comprising potential targets. RNA sequencing results showed that GAS5 was upregulated in five familial Alzheimer's disease (5×FAD) mice, APPswe/PSEN1dE9 (APP/PS1) mice, Alzheimer's disease-related APPswe cells, and serum from patients with Alzheimer's disease. Functional experiments with targeted overexpression and silencing demonstrated that GAS5 played a role in cognitive dysfunction and multiple Alzheimer's disease-associated pathologies, including tau hyperphosphorylation, amyloid-beta accumulation, and neuronal apoptosis. Mechanistic studies indicated that GAS5 acted as an endogenous sponge by competing for microRNA-23b-3p (miR-23b-3p) binding to regulate its targets glycogen synthase kinase 3beta (GSK-3ß) and phosphatase and tensin homologue deleted on chromosome 10 (PTEN) expression in an Argonaute 2-induced RNA silencing complex (RISC)-dependent manner. GAS5 inhibited miR-23b-3p-mediated GSK-3ß and PTEN cascades with a feedforward PTEN/protein kinase B (Akt)/GSK-3ß linkage. Furthermore, recovery of GAS5/miR-23b-3p/GSK-3ß/PTEN pathways relieved Alzheimer's disease-like symptoms in vivo, indicated by the amelioration of spatial cognition, neuronal degeneration, amyloid-beta load, and tau phosphorylation. Together, these findings suggest that GAS5 promotes Alzheimer's disease pathogenesis. This study establishes the functional convergence of the GAS5/miR-23b-3p/GSK-3ß/PTEN pathway on multiple pathologies, suggesting a candidate therapeutic target in Alzheimer's disease.
ABSTRACT
Coiled-coil domain containing 88C (CCDC88C) is a component of non-canonical Wnt signaling, and its dysregulation causes colorectal cancer metastasis. Dysregulated expression of CCDC88C was observed in lymph node metastatic tumor tissues of breast cancer. However, the role of CCDC88C in breast cancer metastasis remains unclear. To address this, the stable BT549 and SKBR3 cell lines with CCDC88C overexpression or knockdown were developed. Loss/gain-of-function experiments suggested that CCDC88C drove breast cancer cell motility in vitro and lung and liver metastasis in vivo. We found that CCDC88C led to c-JUN-induced transcription activation. Overlapping genes were identified from the genes modulated by CCDC88C and c-JUN. CEMIP, one of these overlapping genes, has been confirmed to confer breast cancer metastasis. We found that CCDC88C regulated CEMIP mRNA levels via c-JUN and it exerted pro-metastatic capabilities in a CEMIP-dependent manner. Moreover, we identified the CCDC88C as a substrate of polypeptide N-acetylgalactosaminyltransferase 6 (GALNT6). GALNT6 was positively correlated with CCDC88C protein abundance in the normal breast and breast cancer tissues, indicating that GALNT6 might be associated with expression patterns of CCDC88C in breast cancer. Our data demonstrated that GALNT6 maintained CCDC88C stability by promoting its O-linked glycosylation, and the modification was critical for the pro-metastatic potential of CCDC88C. CCDC88C also could mediate the pro-metastatic potential of GALNT6 in breast cancer. Collectively, our findings uncover that CCDC88C may increase the risk of breast cancer metastasis and elucidate the underlying molecular mechanisms.
ABSTRACT
Essential thrombocythemia (ET) and prefibrotic primary myelofibrosis (pre-PMF) are Philadelphia chromosome-negative myeloproliferative neoplasms. These conditions share overlapping clinical presentations; however, their prognoses differ significantly. Current morphological diagnostic methods lack reliability in subtype differentiation, underlining the need for improved diagnostics. The aim of this study was to investigate the multi-omics alterations in bone marrow biopsies of patients with ET and pre-PMF to improve our understanding of the nuanced diagnostic characteristics of both diseases. We performed proteomic analysis with 4D direct data-independent acquisition and microbiome analysis with 2bRAD-M sequencing technology to identify differential protein and microbe levels between untreated patients with ET and pre-PMF. Laboratory and multi-omics differences were observed between ET and pre-PMF, encompassing diverse pathways, such as lipid metabolism and immune response. The pre-PMF group showed an increased neutrophil-to-lymphocyte ratio and decreased high-density lipoprotein and cholesterol levels. Protein analysis revealed significantly higher CXCR2, CXCR4, and MX1 levels in pre-PMF, while APOC3, APOA4, FABP4, C5, and CFB levels were elevated in ET, with diagnostic accuracy indicated by AUC values ranging from 0.786 to 0.881. Microbiome assessment identified increased levels of Mycobacterium, Xanthobacter, and L1I39 in pre-PMF, whereas Sphingomonas, Brevibacillus, and Pseudomonas_E were significantly decreased, with AUCs for these genera ranging from 0.833 to 0.929. Our study provides preliminary insights into the proteomic and microbiome variations in the bone marrow of patients with ET and pre-PMF, identifying specific proteins and bacterial genera that warrant further investigation as potential diagnostic indicators. These observations contribute to our evolving understanding of the multi-omics variations and possible mechanisms underlying ET and pre-PMF.
Subject(s)
Bone Marrow , Primary Myelofibrosis , Proteomics , Thrombocythemia, Essential , Female , Humans , Male , Middle Aged , Biopsy , Bone Marrow/pathology , Bone Marrow/microbiology , Diagnosis, Differential , Microbiota , Multiomics , Primary Myelofibrosis/pathology , Thrombocythemia, Essential/pathology , Thrombocythemia, Essential/diagnosis , Thrombocythemia, Essential/geneticsABSTRACT
Golgi protein 73 (GP73), a resident protein of the Golgi apparatus, is notably elevated in hepatocellular carcinoma (HCC). While its critical role in remodeling the tumor microenvironment (TME) is recognized, the intricate mechanisms are not fully understood. This study reveals that GP73 in HCC cells interacts with prolyl hydroxylase-2 (PHD-2) in a competitive manner, thereby impeding the hydroxylation of hypoxia-induced factor-1α (HIF-1α). The effect above promotes the production and secretion of vascular endothelial growth factor A (VEGFA). Moreover, exosomal GP73 derived from HCC cells can be internalized by human umbilical vein endothelial cells (HUVECs) and competitively interact with HECTD1, an E3 ubiquitin ligase targeting growth factor receptor-bound protein 2 (GRB2). This interaction stabilizes GRB2, thereby activating the Ras-mitogen-activated protein kinase (MAPK) signaling pathway. Consequently, escalated levels of GP73 intensify VEGF production in HCC cells and potentiate mitogenic signaling in vascular endothelial cells, fostering angiogenesis in the TME. Our findings propose that GP73 might serve as a novel target for anti-angiogenic therapy in HCC.
ABSTRACT
BACKGROUND: Postoperative pulmonary complications (PPCs) after one-lung ventilation (OLV) significantly impact patient prognosis and quality of life. OBJECTIVE: To study the impact of an optimal inspiratory flow rate on PPCs in thoracic surgery patients. METHODS: One hundred eight elective thoracic surgery patients were randomly assigned to 2 groups in this consort study (control group: n = 53 with a fixed inspiratory expiratory ratio of 1:2; and experimental group [flow rate optimization group]: n = 55). Measurements of Ppeak, Pplat, PETCO2, lung dynamic compliance (Cdyn), respiratory rate, and oxygen concentration were obtained at the following specific time points: immediately after intubation (T0); immediately after starting OLV (T1); 30 min after OLV (T2); and 10 min after 2-lung ventilation (T4). The PaO2:FiO2 ratio was measured using blood gas analysis 30 min after initiating one-lung breathing (T2) and immediately when OLV ended (T3). The lung ultrasound score (LUS) was assessed following anesthesia and resuscitation (T5). The occurrence of atelectasis was documented immediately after the surgery. PPCs occurrences were noted 3 days after surgery. RESULTS: The treatment group had a significantly lower total prevalence of PPCs compared to the control group (3.64% vs. 16.98%; P = 0.022). There were no notable variations in peak airway pressure, airway plateau pressure, dynamic lung compliance, PETCO2, respiratory rate, and oxygen concentration between the two groups during intubation (T0). Dynamic lung compliance and the oxygenation index were significantly increased at T1, T2, and T4 (P < 0.05), whereas the CRP level and number of inflammatory cells decreased dramatically (P < 0.05). CONCLUSION: Optimizing inspiratory flow rate and utilizing pressure control ventilation -volume guaranteed (PCV-VG) mode can decrease PPCs and enhance lung dynamic compliance in OLV patients.
Subject(s)
One-Lung Ventilation , Postoperative Complications , Humans , Male , Female , Middle Aged , Postoperative Complications/prevention & control , One-Lung Ventilation/methods , Aged , Thoracic Surgical Procedures/adverse effects , Thoracic Surgical Procedures/methods , Lung Diseases/prevention & control , Lung Diseases/etiology , Lung Diseases/physiopathology , Lung/physiopathology , Prospective StudiesABSTRACT
The cell membrane, consisting of a phospholipid bilayer, is an important defense system of lactic acid bacteria (LAB) against adverse conditions. However, this membrane gets damaged during the process of spray drying of LAB into powder. In this study, two strains of Lactobacillus bulgaricus L9-7 and L4-2-12 with significantly different survival rates of about 22.49% and 0.43% after spray drying were explored at the cell membrane level. A total of 65 significantly different lipid species were screened from the cell membranes of two strains, with cardiolipin (CL) 15:1_22:6_24:0_28:0 being the crucial lipid species affecting membrane resistance. Finally, the KEGG enrichment analysis revealed that glycerophospholipid metabolism was the most predominant pathway, and eleven lipid species were annotated, including CL. Overall, this paper provides valuable insights into enhancing the heat tolerance of LAB.
ABSTRACT
Antimony (Sb) is an attractive anode material for potassium-ion batteries (PIBs), but it suffers from aggregation during the charging-discharging process, thus causing embedded active sites and collapsed structure. The analogous chelation refers to the reaction in which the central nanoparticle is linked to the matrix through multiple coordination bonds to form a stable composite. This strategy can inhibit aggregation and maintain the nanosized structure of Sb, thus activating the utilization of Sb active sites and structural stability. Given the special position of nitrogen (N) in the periodic table of elements and the strong bond energy of Sb-N, the N element can serve as an intermediate to connect Sb nanoparticles and an intrinsic N-doped carbon network via strong Sb-N-C/Sb-NâC covalent bonds using analogous chelation. Herein, a hybrid material of Sb@CTF-NC is fabricated via analogous chelation. The Sb atoms exposed on the surface of Sb nanoparticles are used to chelate with the N-doped carbon for high-performance PIBs. The mechanism underwent ex situ characterizations. The calculation of density functional theory reveals that the increase of adsorption energy and reduction of the K+ diffusion barrier accelerate the electrochemical reaction kinetics.
ABSTRACT
BACKGROUND: Integrated vascular surgery residency positions have doubled more than the last decade. Studies have investigated the impact of co-existing subspecialty surgical training programs on case volume of general surgery residents (GSRs). However, no studies have explored the impact of subspecialty training on GSR operative competency. The aim of this study is to understand the impact of integrated residencies on operative performance and autonomy of GSR performing vascular procedures. METHODS: Autonomy and performance ratings of GSR participating in vascular surgery cases were collected from all institutions participating in the Society for Improving Medical Professional Learning application database from 2015 to 2023. Faculty and self-assessments of autonomy and performance on vascular cases performed by GSRs at programs with co-existing vascular integrated residency (VIR), vascular surgery fellowship (VSF), or no subspecialty vascular training (VX) were compared using Fisher's exact tests with Bonferroni corrections across training levels and case complexity. RESULTS: Eleven thousand one hundred seventy five assessments (26% at institutions with VIR, 46% VSF, and 28% VX) were submitted by 920 GSRs and 343 faculty. Senior GSRs at programs with VSF achieved lower autonomy than those with VIR (P = 0.049) or VX (P = 0.042) based on faculty assessment. GSRs achieved a level of "practice ready" at significantly higher rates when training at programs with VIR, and at the lowest rates with VSF (P < 0.001). However, self-perception of autonomy and performance was highest among GSRs at programs with VX compared with VIR and VSF (P < 0.001). CONCLUSIONS: The presence of VIR was associated with higher achievement of "practice ready" competency and higher levels of operative autonomy among senior GSRs performing vascular procedures. Shared-learning among peers and faculty expertise in teaching resident-level trainees may contribute to this finding.