Poly (ADP-ribose) polymerase 1 promotes HuR/ELAVL1 cytoplasmic localization and inflammatory gene expression by regulating p38 MAPK activity.

Post-transcriptional regulation of cytokine/chemokine mRNA turnover is critical for immune processes and contributes to the mammalian cellular response to diverse inflammatory stimuli. The ubiquitous RNA-binding protein human antigen R (HuR) is an integral regulator of inflammation-associated mRNA fate. HuR function is regulated by various post-translational modifications that alter its subcellular localization and ability to stabilize target mRNAs. Both poly (ADP-ribose) polymerase 1 (PARP1) and p38 mitogen-activated protein kinases (MAPKs) have been reported to regulate the biological function of HuR, but their specific regulatory and crosstalk mechanisms remain unclear. In this study, we show that PARP1 acts via p38 to synergistically promote cytoplasmic accumulation of HuR and stabilization of inflammation-associated mRNAs in cells under inflammatory conditions. Specifically, p38 binds to auto-poly ADP-ribosylated (PARylated) PARP1 resulting in the covalent PARylation of p38 by PARP1, thereby promoting the retention and activity of p38 in the nucleus. In addition, PARylation of HuR facilitates the phosphorylation of HuR at the serine 197 site mediated by p38, which then increases the translocation of HuR to the cytoplasm, ultimately stabilizing the inflammation-associated mRNA expression at the post-transcriptional level.

Analysis of Effect of Quality Control Circle Management Model on the Error Rate of Disposable Item Distribution and Efficiency of Medical Workers in Sterilization Supply Center.

Objective: To explore the effectiveness of quality control circle (QCC) management model in reducing the error rate of dispensing disposable items. Methods: Our hospital's sterilization supply center implemented QCC management model from May 2021 to December 2021 to compare the error rate of disposable items dispensed before and after the implementation of the QCC activities. Results: The one-time item dispensing error rate was lower after the QCC activities, the order claim error rate, print order error rate, and inventory error rate were also reduced, and the required loading time and delivery time were shortened (P < .05). Conclusion: QCC activities can reduce the error rate of dispensing disposable items, save time, improve efficiency, and enhance clinical satisfaction.

The RopGEF Gene Family and Their Potential Roles in Responses to Abiotic Stress in Brassica rapa.

Guanine nucleotide-exchange factors (GEFs) genes play key roles in plant root and pollen tube growth, phytohormone responses, and abiotic stress responses. RopGEF genes in Brassica rapa have not yet been explored. Here, GEF genes were found to be distributed across eight chromosomes in B. rapa and were classified into three subfamilies. Promoter sequence analysis of BrRopGEFs revealed the presence of cis-elements characteristic of BrRopGEF promoters, and these cis-elements play a role in regulating abiotic stress tolerance and stress-related hormone responses. Organ-specific expression profiling demonstrated that BrRopGEFs were ubiquitously expressed in all organs, especially the roots, suggesting that they play a role in diverse biological processes. Gene expression analysis revealed that the expression of BrRopGEF13 was significantly up-regulated under osmotic stress and salt stress. RT-qPCR analysis revealed that the expression of BrRopGEF13 was significantly down-regulated under various types of abiotic stress. Protein-protein interaction (PPI) network analysis revealed interactions between RopGEF11, the homolog of BrRopGEF9, and the VPS34 protein in Arabidopsis thaliana, as well as interactions between AtRopGEF1, the homolog of BrRopGEF13 in Arabidopsis, and the ABI1, HAB1, PP2CA, and CPK4 proteins. VPS34, ABI1, HAB1, PP2CA, and CPK4 have previously been shown to confer resistance to unfavorable environments. Overall, our findings suggest that BrRopGEF9 and BrRopGEF13 play significant roles in regulating abiotic stress tolerance. These findings will aid future studies aimed at clarifying the functional characteristics of BrRopGEFs.

ZNFX1 antisense RNA1 promotes antiviral innate immune responses via modulating ZNFX1 function.

Increasing evidence suggests that natural antisense transcriptional lncRNAs regulate their adjacent coding genes to mediate diverse aspects of biology. Bioinformatics analysis of the previously identified antiviral gene ZNFX1 revealed neighboring lncRNA ZFAS1 transcribed on the opposite strand from ZNFX1. Whether ZFAS1 exerts antiviral function via regulating the dsRNA sensor ZNFX1 is unknown. Here we found that ZFAS1 was upregulated by RNA and DNA viruses and type I IFNs (IFN-I) dependent on Jak-STAT signaling, similar to the transcription regulation of ZNFX1. Knockdown of endogenous ZFAS1 partially facilitated viral infection, while ZFAS1 overexpression showed opposite effects. In addition, mice were more resistant to VSV infection with the delivery of human ZFAS1. We further observed that ZFAS1 knockdown significantly inhibited IFNB1 expression and IFR3 dimerization, whereas ZFAS1 overexpression positively regulated antiviral innate immune pathways. Mechanistically, ZFAS1 positively regulated ZNFX1 expression and antiviral function by enhancing the protein stability of ZNFX1, thereby establishing a positive feedback loop to enhance antiviral immune activation status. In short, ZFAS1 is a positive regulator of antiviral innate immune response via regulating its neighbor gene ZNFX1, adding new mechanistic insight into lncRNA-mediated regulation of signaling in innate immunity.

HSP90.2 modulates 2Q2-mediated wheat resistance against powdery mildew.

Wheat (Triticum aestivum L.) is a critical food crop feeding the world, but pathogens threaten its production. Wheat Heat Shock Protein 90.2 (HSP90.2) is a pathogen-inducible molecular chaperone folding nascent preproteins. Here, we used wheat HSP90.2 to isolate clients regulated at the posttranslational level. Tetraploid wheat hsp90.2 knockout mutant was susceptible to powdery mildew, while the HSP90.2 overexpression line was resistant, suggesting that HSP90.2 was essential for wheat resistance against powdery mildew. We next isolated 1500 clients of HSP90.2, which contained a wide variety of clients with different biological classifications. We utilized 2Q2, a nucleotide-binding leucine repeat-rich protein, as a model to investigate the potential of HSP90.2 interactome in fungal resistance. The transgenic line co-suppressing 2Q2 was more susceptible to powdery mildew, suggesting 2Q2 as a novel Pm-resistant gene. The 2Q2 protein resided in chloroplasts, and HSP90.2 played a critical role in the accumulation of 2Q2 in thylakoids. Our data provided over 1500 HSP90.2 clients with a potential regulation at the protein folding process and contributed a nontypical approach to isolate pathogenesis-related proteins.

Identification of Apiaceae using ITS, ITS2 and psba-trnH barcodes.

Apiaceae plants are used as medicinal herbs, pesticides, spices, and vegetables; thus, accurately identifying Apiaceae species is important. The grassland ecosystem of Heilongjiang Province in northern China has huge reserves of wild Apiaceae plants, but few reports have systematically documented their diversity. In this study, 275 Apiaceae plants of 23 species in 18 genera were collected from this area. We identified Apiaceae species by using nuclear internal transcribed spacer (ITS/ITS2) and psbA-trnH (chloroplast non-coding region) sequences based on experimental data. The identification efficiency of ITS, ITS2 and psbA-trnH sequences was determined and evaluated by sequence alignment and analysis, intraspecific and interspecific genetic distance analyses, and phylogenetic tree construction. ITS, ITS2 could distinguish 21 species from 17 genera of Apiaceae with good identification effect. When identifying species in the Apiaceae family, ITS2 can be used as the core barcode and psbA-trnH can be used as the supplementary barcode. These results can enrich the reference Apiaceae DNA barcode database.

Scoparone suppresses mitophagy-mediated NLRP3 inflammasome activation in inflammatory diseases.

Recent evidence shows that targeting NLRP3 inflammasome activation is an important means to treat inflammasome-driven diseases. Scoparone, a natural compound isolated from the Chinese herb Artemisia capillaris Thunb, has anti-inflammatory activity. In this study we investigated the effect of scoparone on NLRP3 inflammasome activation in inflammatory diseases. In LPS-primed, ATP or nigericin-stimulated mouse macrophage J774A.1 cells and bone marrow-derived macrophages (BMDMs), pretreatment with scoparone (50 µM) markedly restrained canonical and noncanonical NLRP3 inflammasome activation, evidenced by suppressed caspase-1 cleavage, GSDMD-mediated pyroptosis, mature IL-1ß secretion and the formation of ASC specks. We then conducted a transcriptome analysis in scoparone-pretreated BMDMs, and found that the differentially expressed genes were significantly enriched in mitochondrial reactive oxygen species (ROS) metabolic process, mitochondrial translation and assembly process, as well as in inflammatory response. We demonstrated in J774A.1 cells and BMDMs that scoparone promoted mitophagy, a well-characterized mechanism to control mitochondrial quality and reduce ROS production and subsequent NLRP3 inflammasome activation. Mitophagy blockade by 3-methyladenine (3-MA, 5 mM) reversed the protective effects of scoparone on mitochondrial damage and inflammation in the murine macrophages. Moreover, administration of scoparone (50 mg/kg) exerted significant preventive effects via inhibition of NLRP3 activation in mouse models of bacterial enteritis and septic shock. Collectively, scoparone displays potent anti-inflammatory effects via blocking NLRP3 inflammasome activation through enhancing mitophagy, highlighting a potential action mechanism in treating inflammasome-related diseases for further clinical investigation.

Capsaicin functions as a selective degrader of STAT3 to enhance host resistance to viral infection.

Although STAT3 has been reported as a negative regulator of type I interferon (IFN) signaling, the effects of pharmacologically inhibiting STAT3 on innate antiviral immunity are not well known. Capsaicin, approved for the treatment of postherpetic neuralgia and diabetic peripheral nerve pain, is an agonist of transient receptor potential vanilloid subtype 1 (TRPV1), with additional recognized potencies in anticancer, anti-inflammatory, and metabolic diseases. We investigated the effects of capsaicin on viral replication and innate antiviral immune response and discovered that capsaicin dose-dependently inhibited the replication of VSV, EMCV, and H1N1. In VSV-infected mice, pretreatment with capsaicin improved the survival rate and suppressed inflammatory responses accompanied by attenuated VSV replication in the liver, lung, and spleen. The inhibition of viral replication by capsaicin was independent of TRPV1 and occurred mainly at postviral entry steps. We further revealed that capsaicin directly bound to STAT3 protein and selectively promoted its lysosomal degradation. As a result, the negative regulation of STAT3 on the type I IFN response was attenuated, and host resistance to viral infection was enhanced. Our results suggest that capsaicin is a promising small-molecule drug candidate, and offer a feasible pharmacological strategy for strengthening host resistance to viral infection.

Methane Activation by (MoO3 )5 O- Cluster Anions: The Importance of Orbital Orientation.

The reactivity of the molybdenum oxide cluster anion (MoO3 )5 O- , bearing an unpaired electron at a bridging oxygen atom (Ob .- ), towards methane under thermal collision conditions has been studied by mass spectrometry and density functional theory calculations. This reaction follows the mechanism of hydrogen atom transfer (HAT) and is facilitated by the Ob .- radical center. The reactivity of (MoO3 )5 O- can be traced back to the appropriate orientation of the lowest unoccupied molecular orbitals (LUMO) that is essentially the 2p orbital of the Ob .- atom. This study not only makes up the blank of thermal methane activation by the Ob .- radical on negatively charged clusters but also yields new insights into methane activation by the atomic oxygen radical anions.

Occurrence and Cytotoxicity of Aliphatic and Aromatic Halogenated Disinfection Byproducts in Indoor Swimming Pool Water and Their Incoming Tap Water.

Disinfection byproducts (DBPs) in swimming pool water are of wide concern for public health. In this study, the occurrence of five categories of aliphatic halogenated DBPs, i.e., trihalomethanes (THMs), haloacetic acids (HAAs), haloacetonitriles (HANs), halonitromethanes (HNMs), and haloketones (HKs), and six categories of aromatic halogenated DBPs, i.e., halophenols (HPs), halonitrophenols (HNPs), halohydroxy-benzaldehydes (HBALs), halohydroxybenzoic acids (HBAs), halobenzoquinones (HBQs), and haloanilines (HAs), was examined in seven indoor swimming pool water and their incoming tap water. The correlations between the DBP concentrations and water quality parameters were explored. Moreover, the cytotoxicity of the aliphatic and aromatic halogenated DBPs was tested with human hepatoma (HepG2) cells, and the concentration-cytotoxicity contributions of different DBP categories were calculated. The results demonstrate that 24 aliphatic (5 THMs, 8 HAAs, 5 HANs, 4 HNMs, and 2 HKs) and 50 aromatic halogenated DBPs (9 HPs, 8 HNPs, 9 HBALs, 8 HBAs, 11 HBQs, and 5 HAs) were present in the swimming pool water, among which 41 aromatic halogenated DBPs were detected in swimming pool water for the first time. The average concentrations of the five categories of aliphatic halogenated DBPs in the swimming pool water were in the order of HAAs > HANs > HKs > THMs > HNMs, while those in their incoming tap water were in the order of THMs > HAAs > HKs > HANs > HNMs. The average concentrations of the aromatic halogenated DBPs in the swimming pool water were significantly lower than those of the aliphatic halogenated DBPs, following the order of HBQs > HPs > HBAs > HBALs > HAs > HNPs, while those in their incoming tap water were in the order of HBALs > HBQs > HPs > HBAs > HAs > HNPs. The average concentration-cytotoxicity contributions of different DBP categories in the swimming pool water followed the order of HAAs > HANs > HNMs > HKs > HBQs > THMs > HPs > HNPs > HBAs > HBALs > HAs, with HAAs, HANs, and HNMs possessing the main concentration-cytotoxicity contributions (93.2% in total) among all DBP categories.

Monitoring the Dynamic Regulation of the Mitochondrial GTP-to-GDP Ratio with a Genetically Encoded Fluorescent Biosensor.

The interconversion of guanosine triphosphate (GTP) and guanosine diphosphate (GDP) is known to be integral to a wide variety of biological cellular activities, yet to date there are no analytical methods available to directly detect the ratio of intracellular GTP to GDP. Herein, we report GRISerHR, a genetically encoded fluorescent biosensor to monitor the GTP : GDP ratio in multiple cell types and in various organelles under metabolic perturbation. Additionally, we characterized the differential mitochondrial GTP : GDP ratios resulting from genetic modulation of two isoforms of a tricarboxylic acid (TCA) cycle enzyme (succinyl-CoA synthetase; SCS-ATP and SCS-GTP) and of a phosphoenolpyruvate (PEP) cycle enzyme (PEPCK-M). Thus, our GRISerHR sensor achieves spatiotemporally precise detection of dynamic changes in the endogenous GTP : GDP ratio in living cells and can help deepen our understanding about the energy metabolic contributions of guanosine nucleotides in biology.

Emergency stress management among nurses: A lesson from the COVID-19 outbreak in China-a cross-sectional study.

AIMS AND OBJECTIVES: To assess the level of stress response, self-efficacy and perceived social support status of working nurses during the outbreak of the COVID-19 and investigate potential factors affecting their stress. BACKGROUND: The stress level of clinical nurses directly affects their physical and mental health and work efficiency. DESIGN: This study was a cross-sectional investigation, which was performed following the STROBE checklist. The current study was conducted in February 2020 by selecting clinical nurses from the Zigong First People's Hospital for investigation. METHODS: At the peak of the COVID-19 outbreak in China, we assessed clinical nurses with the Stanford Acute Stress Reaction Questionnaire, the General Self-Efficacy Scale and the Perceived Social Support Scale. Specifically, the nurses were divided into three groups: (a) nurses supporting Wuhan; (b) nurses in the department of treating the COVID-19 patients in our hospital (epidemic department); and (c) nurses in the general department without the COVID-19 patients in our hospital (non-epidemic department). RESULTS: A total of 1092 clinical nurses were surveyed with 94 nurses in Wuhan, 130 nurses treating COVID-19 patients in our hospital and 868 nurses working without direct contact with diagnosed COVID-19 patients. The mean stress score of all surveyed nurses was 33.15 (SD: 25.551). There was a statistically significant difference in stress response scores between different departments. Noticeably, the nurses who went to support in Wuhan showed a weaker stress response than the nurses who stayed in our hospital (mean: 19.98 (Wuhan) vs. 32.70 (epidemic department in our hospital) vs. 34.64 (non-epidemic department in our hospital)). In addition, stress was negatively correlated with general self-efficacy and perceived social support. CONCLUSION: The present study suggested that the stress status of second-line nurse without direct contact with diagnosed COVID-19 patients was more severe than that of first-line nurses who had direct contact with COVID-19 patients. RELEVANCE TO CLINICAL PRACTICE: Our study indicated the importance of psychological status of second-line medical staff during the global pandemic.

A Ratiometric Fluorescent Biosensor Reveals Dynamic Regulation of Long-Chain Fatty Acyl-CoA Esters Metabolism.

Despite increasing awareness of the biological impacts of long-chain fatty acyl-CoA esters (LCACoAs), our knowledge about the subcellular distribution and regulatory functions of these acyl-CoA molecules is limited by a lack of methods for detecting LCACoAs in living cells. Here, we report development of a genetically encoded fluorescent sensor that enables ratiometric quantification of LCACoAs in living cells and subcellular compartments. We demonstrate how this FadR-cpYFP fusion "LACSer sensor" undergoes LCACoA-induced conformational changes reflected in easily detectable fluorescence responses, and show proof-of-concept for real-time monitoring of LCACoAs in human cells. Subsequently, we applied LACSer in scientific studies investigating how disruption of ACSL enzymes differentially reduces cytosolic and mitochondrial LCACoA levels, and show how genetic disruption of an acyl-CoA binding protein (ACBP) alters mitochondrial accumulation of LCACoAs.

APEX2-based Proximity Labeling of Atox1 Identifies CRIP2 as a Nuclear Copper-binding Protein that Regulates Autophagy Activation.

Mammalian cell nuclei contain copper, and cancer cells are known to accumulate aberrantly high copper levels, yet the mechanisms underlying nuclear accumulation and copper's broader functional significance remain poorly understood. Here, by combining APEX2-based proximity labeling focused on the copper chaperone Atox1 with mass spectrometry we identified a previously unrecognized nuclear copper binding protein, Cysteine-rich protein 2 (CRIP2), that interacts with Atox1 in the nucleus. We show that Atox1 transfers copper to CRIP2, which induces a change in CRIP2's secondary structure that ultimately promotes its ubiquitin-mediated proteasomal degradation. Finally, we demonstrate that depletion of CRIP2-as well as copper-induced CRIP2 degradation-elevates ROS levels and activates autophagy in H1299 cells. Thus, our study establishes that CRIP2 as an autophagic suppressor protein and implicates CRIP2-mediated copper metabolism in the activation of autophagy in cancer cells.

Galectin-3 knock down inhibits cardiac ischemia-reperfusion injury through interacting with bcl-2 and modulating cell apoptosis.

Acute myocardial infarction (AMI) is a fetal cardiovascular disease with high morbidity and mortality worldwide. In the present study, we elucidated the role of galectin-3 in preventing myocardial ischemic reperfusion injury. We found that galactin-3 was significantly up-regulated in the myocardium and cardiomyocyte subjected to ischemia/reperfusion (I/R) and hypoxia/reoxygenation (H/R) treatment, respectively. Galectin-3 knockdown significantly decreased the ischemic size of the left ventricular and the apoptosis of cardiomyocytes. Moreover, galectin-3 knockdown reversed the decrease of mitochondrial membrane potential and inhibited the inflammation response in myocardium and cultured cardiomyocyte induced by I/R and H/R, respectively. Further, this study revealed that galectin-3 interacted with bcl-2, instead of bax, in the cardiomyocyte, and regulated the phosphorylation of AKT, p70s6k, JNK, IκB and p65. Our findings demonstrated that galectin-3 could prevent myocardial I/R injury through interacting with bcl-2.

MicroRNA-27 attenuates pressure overload-Induced cardiac hypertrophy and dysfunction by targeting galectin-3.

Cardiac hypertrophy is an adaptive response to hemodynamic stress to compensate for cardiac dysfunction. MicroRNAs can regulate cardiac function and play a vital role in the regulation of cardiac hypertrophy. In the current study, in vivo and vitro hypertrophy models are established to explore the role of miR-27b and to elucidate the underlying mechanism in cardiac hypertrophy. Expression of miR-27b was down-regulated in mice with cardiac hypertrophy. The cardiac function of the mice with cardiac hypertrophy could be restored with the overexpression of miR-27b, this is observed in terms of decreasing LVEDd, LVESd, and increasing LVFS, LVEF. This study also predicted and confirmed that galectin-3 is a target gene of miR-27b. Depletion of galectin-3 significantly attenuated hypertrophy of hearts in both in vitro and in vivo tests. In conclusion, MiR-27b be used to exert a protective role against cardiac dysfunction and hypertrophy by decreasing the expression level of galectin-3. The methodology suggested in this study provides a novel therapeutic strategy against cardiac hypertrophy.

Formation and Decomposition of New Iodinated Halobenzoquinones during Chloramination in Drinking Water.

Previously four chlorinated and brominated halo-benzoquinones were reported as new disinfection byproducts (DBPs) in drinking water, which have drawn great concern due to their high toxicity. In this study, three new iodinated halobenzoquinones, including 2-chloro-6-iodo-1,4-benzoquinone (2,6-CIBQ), 2-bromo-6-iodo-1,4-benzoquinone (2,6-BIBQ), and 2,6-diiodo-1,4-benzoquinone (2,6-DIBQ), were detected and identified in drinking water for the first time. Their cytotoxicity was evaluated, and their formation under various conditions was examined. Since they were not stable during chloramination, their further decomposition during chloramination was also explored. The results indicated that the concentrations of 2,6-CIBQ, 2,6-BIBQ, and 2,6-DIBQ in drinking water were in the ranges of 0.7-1.3, 1.8-8.0, and 0.4-15.9 ng/L, respectively. Compared with 2,6-dibromo-1,4-benzoquinone, the iodinated halobenzoquinones were generally more cytotoxic. The formation of 2,6-DIBQ during chloramination was significantly affected by the iodide concentration, pH, and natural organic matter. The five tested iodinated halobenzoquinones decomposed during chloramination following pseudo-first-order decay, with the decomposition rate constants in the rank order of 2,6-CIBQ > 2,6-BIBQ > 2,6-DIBQ > 2,3-diiodo-1,4-benzoquinone >2-iodo-1,4-benzoquinone. Nine polar halogenated intermediates as well as ten aliphatic halogenated DBPs were detected as the decomposition products of 2,6-DIBQ during chloramination, based on which the decomposition pathways of 2,6-DIBQ during chloramination were proposed and verified.

C-N Coupling in N2 Fixation by the Ditantalum Carbide Cluster Anions Ta2C4.

The construction of C-N bonds by the direct incorporation of dinitrogen (N2) instead of ammonia (NH3) into active species is particularly desirable but has been rarely reported. Herein, a ditantalum carbide cluster anion (Ta2C4-) capable of cleaving the N≡N bond and constructing a C-N bond under mild conditions has been identified using mass spectrometry, photoelectron imaging spectroscopy, and quantum-chemical calculations. The photoelectron spectrum of Ta2C4N2- is remarkably different from that of Ta2C4- and matches the simulated spectrum of the Ta2C4N2- species with an end-on-bonded CN unit. The formation of the C-N bond has also been supported by the CN- fragment observed in the collision-induced dissociation of Ta2C4N2-. The exceptional reactivity of Ta2C4- is ascribed to the low-valent metal center serving as an electron reservoir. This study provides a non-NH3 route to construct C-N bonds by incorporating N2 into carbide compounds to produce nitrogenous species.

The effect of low insurance reimbursement on quality of care for non-small cell lung cancer in China: a comprehensive study covering diagnosis, treatment, and outcomes.

BACKGROUND: The insurance reimbursement rate of medical cost affects the quality and quantity of health services provided in China. The nature of this relationship, however, has not been reliably described in the field of non-small cell lung cancer (NSCLC). The objective of the current study was to examine the impact of low reimbursement rates of medical costs on diagnosis, treatment and outcomes among patients with NSCLC. METHODS: We examined care of 2643 NSCLC patients and we divided the study cohort into a high reimbursement rate group and a low reimbursement rate group. The impact of reimbursement rates of medical costs on quality of care of NSCLC patients were examined using logistic regression and generalized linear models. RESULTS: Compared with patients insured with high reimbursement rate, patients insured through lower reimbursement rate programs were less likely to benefit from early detection and treatment services. Delayed detection was more common in low reimbursement group and they were less likely to be recommended for adjuvant chemotherapy, or to receive adjuvant chemotherapy and postoperative radiation therapy and they had lower odds to receipt chemotherapy response assessment. However, low reimbursement rate group had lower rate of in-hospital mortality and metastases. CONCLUSIONS: Low reimbursement rate mainly negatively influenced the diagnosis and treatment of NSCLC. Reducing the gap in reimbursement rate between the three health insurance schemes should be a focus of equalizing access to care and improving the level of medical compliance and finally improving quality of care of NSCLC.

Does Each Atom Count in the Reactivity of Vanadia Nanoclusters?

Vanadium oxide cluster anions (V2O5)nVxOy- (n = 1-31; x = 0, 1; and x + y ≤ 5) with different oxygen deficiencies (Δ = 2y-1-5x = 0, ± 1, and ±2) have been prepared by laser ablation and reacted to abstract hydrogen atoms from alkane molecules (n-butane) in a fast flow reactor. When the cluster size n is less than 25, the Δ = 1 series [(V2O5)nO- clusters] that can contain atomic oxygen radical anions (O•-) generally have much higher reactivity than the other four cluster series (Δ = -2, -1, 0, and 2), indicating that each atom counts in the hydrogen-atom abstraction (HAA) reactivity. Unexpectedly, all of the five cluster series have similar HAA reactivity when the cluster size is greater than 25. The critical dimension of vanadia particles separating the cluster behavior (each atom counts) from the bulk behavior (each atom contributes a little part) is thus about 1.6 nm (∼V50O125). The strong electron-phonon coupling of the vanadia particles has been proposed to create the O•- radicals (V5+ = O2-+ heat → V4+-O•-) for the n > 25 clusters with Δ = -2, -1, 0, and 2. Such a mechanism is supported by a comparative study with the scandium system [(Sc2O3)nScxOy- (n = 1-29; x = 0, 1; and x + y ≤ 4)] for which the Δ = 1 series [(Sc2O3)nO- clusters] always have much higher HAA reactivity than the other cluster series.