Deciphering the Dynamics of EGFR-TKI Resistance in Lung Cancer: Insights from Bibliometric Analysis.

Background: EGFR-TKI resistance poses a significant challenge in the treatment landscape of non-small cell lung cancer (NSCLC), prompting extensive research into mechanisms and therapeutic strategies. In this study, we conduct a bibliometric analysis to elucidate evolving research hotspots and trends in EGFR-TKI resistance, offering insights for clinical interventions and scientific inquiries. Methods: Publications spanning from 1996 to 2024, focusing on EGFR-TKI resistance in NSCLC, were sourced from the Web of Science Core Collection. Utilizing VOSviewer 1.6.19, CiteSpace 6.2. R2, and Scimago Graphica 1.0.35, we analyzed these articles to identify countries/regions and institutions, Journals, publications, key contributors, collaborations, and emerging topics. Results: An analysis of 8051 articles by 38,215 researchers from 86 countries shows growing interest in EGFR-TKI resistance mechanisms. Since 1996, publications have steadily increased, surpassing 500 per year after 2016, with a sharp rise in citations. Research articles make up 84% of publications, emphasizing scholarly focus. Global collaboration, especially among researchers in China, the US, and Japan, is strong. Leading institutions like Dana-Farber and Harvard, along with journals such as "Lung Cancer", are key in sharing findings. Professors Yi-Long Wu and William Pao are prominent contributors. Keyword analysis reveals core themes, including first-generation EGFR-TKIs, emerging agents like osimertinib, and research on the T790M mutation. Conclusion: EGFR-TKI resistance remains a critical issue in NSCLC treatment, driving ongoing research efforts worldwide. Focusing future research on clear identification of resistance mechanisms will guide post-resistance treatment strategies, necessitating further exploration, alongside the validation of emerging drugs through clinical trials. Moreover, "chemo+" treatments following EGFR-TKI resistance require more clinical data and real-world evidence for assessing safety and patient outcomes. As research advances, a multidisciplinary approach will be key to overcoming these challenges. Continued innovation in treatment could greatly enhance patient survival and quality of life.

SMARCA4 mutations and expression in lung adenocarcinoma: prognostic significance and impact on the immunotherapy response.

The switch/sucrose non-fermenting (SWI/SNF) complex family includes important chromatin-remodeling factors that are frequently mutated in lung adenocarcinoma (LUAD). However, the role of one family member, SMARCA4, in LUAD prognosis and immunotherapy sensitivity remains unclear. In the present study, 6745 LUAD samples from the cBioPortal database were used to analyze the relationships between SMARCA4 mutations and patient prognoses and clinical characteristics. Additionally, we examined the correlation between SMARCA4 mutations and prognosis in patients treated with immunotherapy using two immune-related datasets. SMARCA4 mutations and low expression were associated with shorter survival, and mutations were associated with a high tumor mutational burden and high microsatellite instability. SMARCA4 mutations were accompanied by KRAS, KEAP1, TP53 and STK11 mutations. No significant difference was observed in the immunotherapy response between patients with and without SMARCA4 mutations. When KRAS or STK11 mutations were present, immunotherapy effectiveness was poorer; however, when both SMARCA4 and TP53 mutations were present, immunotherapy was more effective. Furthermore, low SMARCA4 expression predicted a higher immunophenoscore, and SMARCA4 expression was correlated with certain immune microenvironment features. Taken together, our results suggest that SMARCA4 mutations and low expression might be associated with poor LUAD prognosis. Additionally, immunotherapy efficacy in patients with SMARCA4 mutations depended on the co-mutant genes. Thus, SMARCA4 could be an important factor to be considered for LUAD diagnosis and treatment.

Uncovering the Intrinsic High Fracture Toughness of Titanium via Lowered Oxygen Impurity Content.

Titanium (Ti) and its alloys are known to exhibit room-temperature fracture toughness below 130 MPa m1/2, only about one half of the best austenitic stainless steels. It is purported that this is not the best possible fracture resistance of Ti, but a result of oxygen impurities that sensitively retard the activities of plasticity carriers in this hexagonal close-packed metal. By a reduction of oxygen content from the 0.14 wt% in commercial purity Ti to 0.02 wt%, the mode-Ι fracture toughness of the low-oxygen Ti is measured to be as high as KJ Ic ≈ 255 MPa m1/2, corresponding to J-integral-based crack-initiation toughness of up to JIc ≈ 537 kJ m-2. This extraordinary toughness, reported here for the first time for pure Ti, places Ti among the toughest known materials. The intrinsic high fracture resistance is attributed to the profuse plastic deformation in a significantly enlarged plastic zone, rendered by the pronounced deformation twinning ahead of the crack tip along with ample twin-stimulated 〈c+a〉 dislocation activities, in the absence of impeding oxygen. Controlling the content of a property-controlling impurity thus holds the promise to be a readily applicable strategy to reach for unprecedented damage tolerance in some other structural alloys.

RNF43 in cancer: Molecular understanding and clinical significance in immunotherapy.

Identifying biomarkers to predict immune checkpoint inhibitor (ICI) efficacy is warranted. Considering that somatic mutation-derived neoantigens induce strong immune responses, patients with a high tumor mutational burden reportedly tend to respond to ICIs. Therefore, the original function of neoantigenic mutations and their impact on the tumor microenvironment (TME) require attention. RNF43 is a type of RING E3 ubiquitin ligase, and long-term survivors in most cancers had conserved patterns of mutations of RNF43. Also, high microsatellite instability patients had a higher RNF43 mutation rate compared with microsatellite stability tumor patients, who were more sensitive to ICI treatment. Therefore, RNF43 has become a promising biomarker of immunotherapy in a wide range of cancers. This review focuses on the up-to-date knowledge of RNF43 mutation in cancer. We summarize the cancer hallmarks involving activities regulated by RNF43 and highlight its extremely sophisticated regulation of WNT signaling and tumor microenvironment. The key genes interacting with RNF43 have also been summarized and discussed. Additionally, we highlight and propose new strategies of targeting RNF43 and RNF43-based combinations with established immunotherapy and combination therapy. These efforts may provide new perspectives for RNF43-based target therapy in cancer.

Preparation, Deformation Behavior and Irradiation Damage of Refractory Metal Single Crystals for Nuclear Applications: A Review.

Refractory metal single crystals have been applied in key high-temperature structural components of advanced nuclear reactor power systems, due to their excellent high-temperature properties and outstanding compatibility with nuclear fuels. Although electron beam floating zone melting and plasma arc melting techniques can prepare large-size oriented refractory metals and their alloy single crystals, both have difficulty producing perfect defect-free single crystals because of the high-temperature gradient. The mechanical properties of refractory metal single crystals under different loads all exhibit strong temperature and crystal orientation dependence. Slip and twinning are the two basic deformation mechanisms of refractory metal single crystals, in which low temperatures or high strain rates are more likely to induce twinning. Recrystallization is always induced by the combined action of deformation and annealing, exhibiting a strong crystal orientation dependence. The irradiation hardening and neutron embrittlement appear after exposure to irradiation damage and degrade the material properties, attributed to vacancies, dislocation loops, precipitates, and other irradiation defects, hindering dislocation motion. This paper reviews the research progress of refractory metal single crystals from three aspects, preparation technology, deformation behavior, and irradiation damage, and highlights key directions for future research. Finally, future research directions are prospected to provide a reference for the design and development of refractory metal single crystals for nuclear applications.

Oxytocin Attenuates Sympathetic Innervation with Inhibition of Cardiac Mast Cell Degranulation in Rats after Myocardial Infarction.

Sympathetic hyperinnervation is the leading cause of fatal ventricular arrhythmia (VA) after myocardial infarction (MI). Cardiac mast cells cause arrhythmias directly through degranulation. However, the role and mechanism of mast cell degranulation in sympathetic remodeling remain unknown. We investigated the role of oxytocin (OT) in stabilizing cardiac mast cells and improving sympathetic innervation in rats. MI was induced by coronary artery ligation. Western blotting, immunofluorescence, and toluidine staining of mast cells were performed to determine the expression and location of target protein. Mast cells accumulated significantly in peri-infarcted tissues and were present in a degranulated state. They expressed OT receptor (OTR), and OT infusion reduced the number of degranulated cardiac mast cells post-MI. Sympathetic hyperinnervation was attenuated as assessed by immunofluorescence for tyrosine hydroxylase (TH). Seven days post-MI, the arrhythmia score of programmed electrical stimulation was higher in vehicle-treated rats with MI than in rats treated with OT. An in vitro study showed that OT stabilized mast cells via the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signaling pathway. Further in vivo studies on OTR-deficient mice showed worsening mast cell degranulation and worsening sympathetic innervation. OT pretreatment inhibited cardiac mast cell degranulation post-MI and prevented sympathetic hyperinnervation, along with mast cell stabilization via the PI3K/Akt pathway. SIGNIFICANCE STATEMENT: This is the first study to elucidate the role and mechanism of oxytocin (OT) in inflammatory-sympathetic communication mediated sympathetic hyperinnervation after myocardial infarction (MI), providing new approaches to prevent fatal arrhythmias.

Competitive-like binding between carbon black and CTNNB1 to ΔNp63 interpreting the abnormal respiratory epithelial repair after injury.

Airway epithelium is extraordinary vulnerable to damage owning to continuous environment exposure. Subsequent repair is therefore essential to restore the homeostasis of respiratory system. Disruptions in respiratory epithelial repair caused by nanoparticles exposure have been linked to various human diseases, yet implications in repair process remain incompletely elucidated. This study aims to elucidate the key stage in epithelial repair disturbed by carbon black (CB) nanoparticles, highlighting the pivotal role of ΔNp63 in mediating the epithelium repair. A competitive-like binding between CB and beta-catenin 1 (CTNNB1) to ΔNp63 is proposed to elaborate the underlying toxicity mechanism. Specifically, CB exhibits a remarkable inhibitory effect on cell proliferation, leading to aberrant airway epithelial repair, as validated in air-liquid culture. ΔNp63 drives efficient epithelial proliferation during CB exposure, and CTNNB1 was identified as a target of ΔNp63 by bioinformatics analysis. Further molecular dynamics simulation reveals that oxygen-containing functional groups on CB disrupt the native interaction of CTNNB1 with ΔNp63 through competitive-like binding pattern. This process modulates CTNNB1 expression, ultimately restraining proliferation during respiratory epithelial repair. Overall, the current study elucidates that the diminished interaction between CTNNB1 and ΔNp63 impedes respiratory epithelial repair in response to CB exposure, thereby enriching the public health risk assessment on CB-related respiratory diseases.

Effect of photodynamic therapy mediated by hematoporphyrin derivatives on small cell lung cancer H446 cells and bronchial epithelial BEAS-2B cells.

To investigate the effects of photodynamic therapy (PDT) mediated by hematoporphyrin derivatives (HPD) on the proliferation of small cell lung cancer H446 cells and bronchial epithelial BEAS-2B cells. H446 cells and BEAS-2B cells were cultured in vitro with different concentrations of HPD(0, 5, 10, 12, 15, 20 µg/mL) for 4 h, and then irradiated with 630 nm laser with different energy densities (0, 25, 50, 75, 100 mW/cm2). Cell viability of H446 cells and BEAS-2B cells were detected by CCK8 assay. The cell apoptosis was observed with Annexin V-FTTC/PI double staining and Hoechst 33258. The RT-PCR examination was applied to detect the transcriptional changes of the mRNA of Bax、Bcl-2, and Caspase-9. The results of CCK8 showed that when the HPD was 15 µg/mL and the laser power density reached 50 mW/cm2, the cell viability was significantly decreased compared with the black control group. Hoechst 33258 staining showed that with the increase of HPD concentration, the cell density was reduced, and apoptotic cells increased. Flow cytometry assay revealed that the apoptotic rates of the HPD-PDT group of H446 cells and BEAS-2B cells were significantly different from those of the blank control group. The RT-PCR examination showed that the expression levels of Bax and Caspase-9 mRNA in the HPD-PDT group were up-regulated, while the expression levels of Bcl-2 mRNA were down-regulated significantly. HPD-PDT can inhibit H446 cells and BEAS-2B cells growth. The mechanism may be related to up-regulating the expression levels of Bax and Caspase-9 mRNA and down-regulating the expression levels of Bcl-2 mRNA.

Efficacy of immunotherapy in HER2-mutated non-small cell lung cancer: a single-arm meta-analysis.

BACKGROUND: Non-small cell lung cancers (NSCLC) harboring Human Epidermal Growth Factor Receptor 2 (HER2) mutations represent a distinct subset with unique therapeutic challenges. Although immune checkpoint inhibitors (ICIs) have been transformative in lung cancer treatment, the efficacy of ICIs in HER2-mutated NSCLC remains to be established. METHODS: We systematically searched for real-world studies investigating the use of ICIs in treating HER2-mutated NSCLC, sourced from the PubMed, Cochrane Library, and Embase databases. Outcomes including objective response rate (ORR), disease control rate (DCR), and progression-free survival (PFS) were extracted for further analysis. RESULTS: Twelve studies involving 260 patients were enrolled in this meta-analysis. Pooled data revealed an ORR of 0.26 (95% CI 0.17-0.34), a DCR of 0.68 (95% CI 0.55-0.81), and a median PFS (mPFS) of 5.36 months (95% CI 3.50-7.21). Notably, in the subgroup receiving combined immune and chemotherapy, the ORR increased to 0.37 (95% CI 0.26-0.49), the DCR to 0.79 (95% CI 0.70-0.87), and the mPFS to 7.10 months (95% CI 5.21-8.99). CONCLUSIONS: ICIs demonstrate promising anti-tumor activity and safety in patients with HER2-mutated NSCLC. Furthermore, the combined regimen of ICIs and chemotherapy may provide a significant therapeutic option for this patient population.

Prognostic implications of neutrophil-to-lymphocyte ratio in patients with extensive-stage small cell lung cancer receiving chemoimmunotherapy: A multicenter, real-world study.

BACKGROUND: Neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) are closely related to the prognosis of patients with non-small cell lung cancer, but their effect on extensive-stage small cell lung cancer (ES-SCLC) remains uncertain. METHODS: This retrospective study was conducted in ES-SCLC patients treated with first-line atezolizumab or durvalumab and platinum-etoposide. Clinical data from three hospitals were analyzed. Significant risk factors for survival were identified using descriptive statistics and Cox regression. Homogeneity was assessed using t-tests or nonparametric tests. Kaplan-Meier analysis revealed an association between high NLR level and median PFS and OS. RESULTS: A total of 300 ES-SCLC patients were included in the study. Cox regression analysis revealed that an elevated NLR level after the second treatment cycle (defined as NLRT2) was an independent prognostic factor for survival. Stratifying patients based on median NLRT2 showed significant differences in both PFS (HR: 1.863, 95% CI: 1.62-2.12, p < 0.001) and OS (HR: 2.581, 95% CI: 2.19-3.04, p < 0.001) between NLR ≥ 1.75 and NLR < 1.75 groups. mPFS and mOS were 8.2 versus 6.1 months and 13.7 versus 9.5 months, respectively. NLR was also associated with treatment efficacy and occurrence of irAEs. Further stratification based on NLR and irAEs showed that in the NLR < 1.75 group, patients with irAEs had prolonged mPFS and mOS. In the NLR ≥ 1.75 group, only mPFS showed a significant difference between patients with and without irAEs. CONCLUSION: NLRT2 and irAEs can predict the prognosis of ES-SCLC patients with first-line ES-SCLC receiving PD-L1 inhibitors combined with chemotherapy.

Effect of a 630 nm light on vasculogenic mimicry in A549 lung adenocarcinoma cells in vitro.

OBJECTIVE: The objective of this study was to investigate the effect of photodynamic therapy (PDT) on the formation of vasculogenic mimicry (VM) in the human lung adenocarcinoma A549 cell line in vitro. METHODS: The participants were divided into a blank control group, a photosensitizer group, a light group, and a PDT group. Cells from each group were cultured in three dimensions using Matrigel, and vasculogenic mimicry generation was observed microscopically. Periodic Acid-Schiff (PAS) staining was used to verify the vasculogenic mimicry structure. Reverse Transcription-Polymerase Chain Reaction (RT-PCR) was used to detect the expression levels of cellular osteopontin (OPN) and vascular endothelial growth factor (VEGF) mRNA. Western blotting was used to detect the expression levels of cellular OPN and VEGF protein. RESULTS: A549 cells cultured on Matrigel for about six hours revealed VM on PAS staining, and the number of formations was significantly reduced in the PDT group compared with other groups (P < 0.05). The RT-PCR results showed that the PDT group downregulated OPN and VEGF mRNA expression compared with each control group (P < 0.05). Western blot results showed that OPN and VEGF protein expression was downregulated in the PDT group compared with each control group (P < 0.05). The results of RT-PCR showed that the expression of OPN and VEGF mRNA was downregulated in the PDT group compared with each control group (P < 0.05). The results of Western blotting showed that the expression of OPN and VEGF was downregulated in the protein PDT group compared with each control group (P < 0.001). CONCLUSION: Photodynamic therapy significantly inhibited the formation of vasculogenic mimicry in human lung adenocarcinoma A549 cells in vitro and downregulated the expression of OPN, VEGF mRNA, and protein levels.

Direct Observation of Vacancy-Cluster-Mediated Hydride Nucleation and the Anomalous Precipitation Memory Effect in Zirconium.

Controlling the heterogeneous nucleation of new phases is of importance in tuning the microstructures and properties of materials. However, the role of vacancy-a popular defect in materials that is hard to be resolved under conventional electron microscopy-in the heterogeneous phase nucleation remains intriguing. Here, this work captures direct in situ experimental evidences that vacancy clusters promote the heterogeneous hydride nucleation and cause the anomalous precipitation memory effect in zirconium. Both interstitial and vacancy dislocation loops form after hydride dissolution. Interestingly, hydride reprecipitation only occurs on those vacancy loop decorated sites during cooling. Atomistic simulations reveal that hydrogen atoms are preferentially segregated at individual vacancy and vacancy clusters, which assist hydride nucleation, and stimulate the unusual memory effect during hydride reprecipitation. The finding breaks the traditional view on the sequence of heterogeneous nucleation sites and sheds light on the solid phase transformation related to vacancy-sensitive alloying elements.

Synthesis by adding CTAB and characterization of Ag@CuO@rGO nanocomposite with a novel core-shell crystal sugar structure and its application in supercapacitors.

In this study, we successfully synthesized Ag@CuO@rGO (rGO wrapped around Ag/CuO) nanocomposites using AgNO3, Cu(NO)32, and NaOH as raw materials and particularly treated CTAB as a template by chemical precipitation, hydrothermal synthesis, and subsequent high-temperature calcination processes. In addition, transmission electron microscopy (TEM) images revealed that the prepared products appeared to have a mixed structure. The results indicated that the best choice was CuO wrapped around Ag nanoparticles to form a core-shell crystal structure, and the crystal particles were arranged similarly to form an icing sugar block structure and were tightly wrapped by rGO. Moreover, the electrochemical test results demonstrated that Ag@CuO@rGO composite electrode material exhibited high pseudocapacitance performance; the material had a high specific capacity of 1453 F g-1 at a current density of 2.5 mA cm-2, and the charging and discharging cycles remained constant up to 2000 times, indicating that the introduction of Ag improved the cycling stability and reversibility of the CuO@rGO electrode material and increased its specific capacitance, leading to the increase in the specific capacitance of supercapacitors. Therefore, the above results strongly support the application of Ag@CuO@rGO in optotronic devices.

Mechanisms of Hydride Nucleation, Growth, Reorientation, and Embrittlement in Zirconium: A Review.

Zirconium (Zr) hydrides threaten the reliability of fuel assembly and have repeatedly induced failures in cladding tubes and pressure vessels. Thus, they attract a broad range of research interests. For example, delayed hydride cracking induced a severe fracture and failure in a Zircaloy-2 pressure tube in 1983, causing the emergency shutdown of the Pickering nuclear reactor. Hydride has high hardness and very low toughness, and it tends to aggregate toward cooler or tensile regions, which initiates localized hydride precipitation and results in delayed hydride cracking. Notably, hydride reorientation under tensile stress substantially decreases the fracture toughness and increases the ductile-to-brittle transition temperature of Zr alloys, which reduces the safety of the long-term storage of spent nuclear fuel. Therefore, improving our knowledge of Zr hydrides is useful for effectively controlling hydride embrittlement in fuel assembly. The aim of this review is to reorganize the mechanisms of hydride nucleation and growth behaviors, hydride reorientation under external stress, and hydride-induced embrittlement. We revisit important examples of progress of research in this field and emphasize the key future aspects of research on Zr hydrides.

Achieving Superior High-Temperature Strength and Oxidation Resistance of TiAl Nanocomposite through In Situ Semicoherent MAX Phase Precipitation.

Increasing the service temperature of TiAl intermetallics is the main challenge for the development of next-generation aircraft. Dispersion-strengthening, an effective means to further improve the high-temperature performance of metals, fails to implement in TiAl intermetallics due to difficulties in interface optimization. Here, we successively fabricate a TiAl naocomposite with fully lamellar microstructures and homogeneously dispersed Ti2AlC nanoprecipitates via spark plasma sintering. The composite consisted of semicoherent interfaces among γ-TiAl/Ti2AlC precipitates/α2-Ti3Al, in addition to continuous polysynthetic nanotwins. Strong pinning effects as well as strain-induced nanoscale TiCr2 precipitation uplift the operation temperature of TiAl nanocomposites by more than 50 °C. Furthermore, we experimentally proved that semicoherent interfaces among in situ Ti2AlC precipitates and its surrounding matrix serve as oxygen diffusion barrier during isothermal oxidization and significantly drop down the mass gain of TiAl nanocomposites during operation, making the present nanocomposite a highly potential candidate for use as light-weight structural materials in automotive and aerospace industries.

Dislocation-Mediated Hydride Precipitation in Zirconium.

The formation of hydrides challenges the integrity of zirconium (Zr) fuel cladding in nuclear reactors. The dynamics of hydride precipitation are complex. Especially, the formation of the butterfly or bird-nest configurations of dislocation structures around hydride is rather intriguing. By in-situ transmission electron microscopy experiments and density functional theory simulations, it is discovered that hydride growth is a hybrid displacive-diffusive process, which is regulated by intermittent dislocation emissions. A strong tensile stress field around the hydride tip increases the solubility of hydrogen in Zr matrix, which prevents hydride growth. Punching-out dislocations reduces the tensile stress surrounding the hydride, decreases hydrogen solubility, reboots the hydride precipitation and accelerates the growth of the hydride. The emission of dislocations mediates hydride growth, and finally, the consecutively emitted dislocations evolve into a butterfly or bird-nest configuration around the hydride.

Relative mobility of screw versus edge dislocations controls the ductile-to-brittle transition in metals.

Body-centered cubic metals including steels and refractory metals suffer from an abrupt ductile-to-brittle transition (DBT) at a critical temperature, hampering their performance and applications. Temperature-dependent dislocation mobility and dislocation nucleation have been proposed as the potential factors responsible for the DBT. However, the origin of this sudden switch from toughness to brittleness still remains a mystery. Here, we discover that the ratio of screw dislocation velocity to edge dislocation velocity is a controlling factor responsible for the DBT. A physical model was conceived to correlate the efficiency of Frank-Read dislocation source with the relative mobility of screw versus edge dislocations. A sufficiently high relative mobility is a prerequisite for the coordinated movement of screw and edge segments to sustain dislocation multiplication. Nanoindentation experiments found that DBT in chromium requires a critical mobility ratio of 0.7, above which the dislocation sources transition from disposable to regeneratable ones. The proposed model is also supported by the experimental results of iron, tungsten, and aluminum.

Atomic-Scale Hidden Point-Defect Complexes Induce Ultrahigh-Irradiation Hardening in Tungsten.

Tungsten displays high strength in extreme temperature and radiation environments and is considered a promising plasma facing material for fusion nuclear reactors. Unlike other metals, it experiences substantial irradiation hardening, which limits service life and presents safety concerns. The origin of ultrahigh-irradiation hardening in tungsten cannot be well-explained by conventional strengthening theories. Here, we demonstrate that irradiation leads to near 3-fold increases in strength, while the usual defects that are generated only contribute less than one-third of the hardening. An analysis of the distribution of tagged atom-helium ions reveals that more than 87% of vacancies and helium atoms are unaccounted for. A large fraction of helium-vacancy complexes are frozen in the lattice due to high vacancy migration energies. Through a combination of in situ nanomechanical tests and atomistic calculations, we provide evidence that irradiation hardening mainly originates from high densities of atomic-scale hidden point-defect complexes.

Current status and influencing factors of nursing interruption events.

OBJECTIVES: To investigate the status of nursing interruption events during medicine administration and to analyze the factors influencing interruptions. STUDY DESIGN: The nursing drug delivery process was divided into 3 segments: the processing of doctors' orders, drug allocation, and bedside drug administration. The frequency, source, type, and outcome of interruption events during these 3 segments were observed. The interruption time and medication errors caused by interruptions were analyzed. METHODS: The structural observation method was used to observe the 3 steps of the drug delivery process. The observations were performed between 8:30 and 10:30 and between 13:30 and 14:30. Count data are described as frequency, composition ratio, and cumulative percentage. R×C contingency table, t tests, and analysis of variance were used to analyze the data. RESULTS: In 270 hours of observation, 3424 nursing interruptions occurred, for a mean of 12.68 interruptions per hour. The mean (SD) interruption time was 28.03 (11.01) seconds, and the total duration of drug administration interruptions was 26.65 hours, accounting for 9.87% of the total observation time. The sources of interruption events were as follows: family members, the environment, doctors, patients, colleagues, the nurses themselves, and others; of these interruptions, 2340 were low-priority events (eg, visitor inquiry, telephone call, consultation, discharge questions), accounting for 68.34%. The incidence of medication errors due to interruptions was 1.139%. CONCLUSIONS: Nursing interruption events occur frequently, come from many sources, have complex causes, and commonly lead to negative outcomes. Interruption also has a time cost and can directly lead to medication errors.

Long non-coding RNA CCAT1 sponges miR-490 to enhance cell proliferation and migration of non-small cell lung cancer.

BACKGROUND: Non-small cell lung cancer (NSCLC) accounts for 85% of lung cancer which is the most frequently diagnosed malignancy in China. Colon cancer associated transcript 1 (CCAT1) acts as an oncogene in enhancing tumor progression. However, the effects of CCAT1 in NSCLC remain unclear. The purpose of this study was to explore the role of CCAT1 in NSCLC. METHODS: Wound healing and transwell assays were performed to measure cell migration. RT-qPCR was employed to calculate the mRNA level of CCAT1 and miR-490. RESULTS: High expression of CCAT1 was observed in NSCLC tissues and cells, with low expression of miR-490. CCAT1 promoted the proliferation and metastasis of H1299 and A549 cells, while miR-490 had the opposite effect. CCAT1 could specifically bind to miR-490 and regulate its expression. MiR-490 partially reversed the inhibitory effect of CCAT1 on cell proliferation and metastasis. CONCLUSIONS: The CCAT1/miR-490 molecular axis has been shown to be important for the treatment of NSCLC.