Fatty Acid Binding Protein-4 Silencing Inhibits Ferroptosis to Alleviate Lipopolysaccharide-induced Injury of Renal Tubular Epithelial Cells by Blocking Janus Kinase 2/Signal Transducer and Activator of Transcription 3 Signaling.

Sepsis-induced kidney injury (SAKI) has been frequently established as a prevailing complication of sepsis which is linked to unfavorable outcomes. Fatty acid-binding protein-4 (FABP4) has been proposed as a possible target for the treatment of SAKI. In the current work, we aimed to explore the role and underlying mechanism of FABP4 in lipopolysaccharide (LPS)-induced human renal tubular epithelial cell damage. In LPS-induced human kidney 2 (HK2) cells, FABP4 expression was tested by the reverse transcription-quantitative polymerase chain reaction and Western blot. Cell counting kit-8 method assayed cell viability. Inflammatory levels were detected using the enzyme-linked immunosorbent assay. Immunofluorescence staining measured the nuclear translocation of nuclear factor kappa B p65. Thiobarbituric acid-reactive substances assay and C11 BODIPY 581/591 probe were used to estimate the level of cellular lipid peroxidation. Fe2+ content was examined by the kit. In addition, the expression of proteins related to inflammation-, ferroptosis- and Janus kinase 2 (JAK2)/signal transducer, and activator of transcription 3 (STAT3) signaling was detected by the Western blot analysis. The results revealed that FABP4 was significantly upregulated in LPS-treated HK2 cells, the knockdown of which elevated the viability, whereas alleviated the inflammation and ferroptosis in HK2 cells challenged with LPS. In addition, down-regulation of FABP4 inactivated JAK2/STAT3 signaling. JAK2/STAT3 stimulator (colivelin) and ferroptosis activator (Erastin) partially restored the effects of FABP4 interference on LPS-triggered inflammation and ferroptosis in HK2 cells. Together, FABP4 knockdown inhibited ferroptosis to alleviate LPS-induced injury of renal tubular epithelial cells through suppressing JAK2/STAT3 signaling.

Ru(II)-Catalyzed Divergent C-H Alkynylation Cascade with Bifunctional α-Alcohol Haloalkynes.

Native functionality directed the C-H activation cascade to enable rapid construction of molecular complexity, featuring step-economy and synthetic efficiency. Herein, by exploiting bifunctional α-alcohol haloalkynes, we developed Ru(II)-catalyzed carboxylic acid, amine, and amide assisted divergent C-H alkynylation and annulation cascade, affording polyfunctional heterocycles. Significantly, a bilateral aryl C-H polycyclization cascade of azobenzenes was achieved using the versatile haloalkynes.

Step-growth Polymerization of Aziridines with Elemental Sulfur: Easy Access to Linear Polysulfides and Their Use as Recyclable Adhesives.

The bulk radical polymerization of bis(aziridine) with molten elemental sulfur resulted in brittle, cross-linked polymers. However, when the bis(aziridine) was treated with elemental sulfur in the presence of an organobase, the ring-opening reaction of aziridine with oligosulfide anions occurred, leading to the formation of linear polymers by step-growth polymerization. These newly synthesized polymers possess repeating units containing a sulfonamide or amide functional moiety and oligosulfide bonds with an average sulfur segment of about two. A small molecular model reaction confirmed the nucleophilic addition reaction of elemental sulfur to aziridine. It was verified that S-S dynamic bond exchange takes place in the presence of an organic base within the linear chains. The mixture of the synthesized polysulfides with pyridine exhibits exceptional adhesive properties when applied to steel, and aluminum substrates. Notably, these prepared adhesives displayed good reusability due to the dynamic S-S exchange and complete recyclability due to their solution processability. This elemental sulfur-involved polymerization approach represents an innovative method for the synthesis of advanced sulfur-containing polymers, demonstrating the potential for various applications in adhesives and beyond.

[Development and validation of a mechanical power-oriented nomogram model for predicting the risk of weaning failure in mechanically ventilated patients: an analysis using the data from MIMIC-IV].

OBJECTIVE: To develop and validate a mechanical power (MP)-oriented nomogram prediction model of weaning failure in mechanically ventilated patients. METHODS: Patients who underwent invasive mechanical ventilation (IMV) for more than 24 hours and were weaned using a T-tube ventilation strategy were collected from the Medical Information Mart for Intensive Care-IV v1.0 (MIMIC-IV v1.0) database. Demographic information and comorbidities, respiratory mechanics parameters 4 hours before the first spontaneous breathing trial (SBT), laboratory parameters preceding the SBT, vital signs and blood gas analysis during SBT, length of intensive care unit (ICU) stay and IMV duration were collected and all eligible patients were enrolled into the model group. Lasso method was used to screen the risk factors affecting weaning outcomes, which were included in the multivariate Logistic regression analysis. R software was used to construct the nomogram prediction model and build the dynamic web page nomogram. The discrimination and accuracy of the nomogram were assessed by receiver operator characteristic curve (ROC curve) and calibration curves, and the clinical validity was assessed by decision curve analysis (DCA). The data of patients undergoing mechanical ventilation hospitalized in ICU of the First People's Hospital of Lianyungang City and the Second People's Hospital of Lianyungang City from November 2021 to October 2022 were prospectively collected to externally validate the model. RESULTS: A total of 3 695 mechanically ventilated patients were included in the model group, and the weaning failure rate was 38.5% (1 421/3 695). Lasso regression analysis finally screened out six variables, including positive end-expiratory pressure (PEEP), MP, dynamic lung compliance (Cdyn), inspired oxygen concentration (FiO2), length of ICU stay and IMV duration, with coefficients of 0.144, 0.047, -0.032, 0.027, 0.090 and 0.098, respectively. Logistic regression analysis showed that the six variables were all independent risk factors for predicting weaning failure risk [odds ratio (OR) and 95% confidence interval (95%CI) were 1.155 (1.111-1.200), 1.048 (1.031-1.066), 0.968 (0.963-0.974), 1.028 (1.017-1.038), 1.095 (1.076-1.113), and 1.103 (1.070-1.137), all P < 0.01]. The MP-oriented nomogram prediction model of weaning failure in mechanically ventilated patients showed accurate discrimination both in the model group and external validation group, with area under the ROC curve (AUC) and 95%CI of 0.832 (0.819-0.845) and 0.879 (0.833-0.925), respectively. Furthermore, its predictive accuracy was significantly higher than that of individual indicators such as MP, Cdyn, and PEEP. Calibration curves showed good correlation between predicted and observed outcomes. DCA indicated that the nomogram model had high net benefits, and was clinically beneficial. CONCLUSIONS: The MP-oriented nomogram prediction model of weaning failure accurately predicts the risk of weaning failure in mechanical ventilation patients and provides valuable information for clinicians making decisions on weaning.

Elastic power, a novel predictor of the severity and prognosis of ARDS.

PURPOSE: To explore the predictive value of the new comprehensive respiratory mechanics parameters elastic power (EP) and elastic power normalized to the compliance (Cst-EP) in the evaluation of the severity and 28-day prognosis of ARDS patients. METHODS: The MIMIC-III database was used to identify ARDS patients under invasive mechanical ventilation for at least 48 h. Their baseline data and ventilatory variables were collected. EP, elastic energy, driving pressure and mechanical power were calculated according to the corresponding formulas. Their value in assessing the severity of ARDS was evaluated. The correlation between Cst-EP and 28-day prognosis of ARDS patients was analyzed. RESULTS: EP was independently associated with the severity of the ARDS and the odds ratio (OR) was 1.301 [95% CI (1.190-1.423), p < 0.001]. It has higher accuracy for the severity of ARDS, with an optimal cut-off value of 14.6 J/min. The Cst-EP was significantly associated with increased risk of death and the hazard ratio (HR) per 100 J/min × cmH2O/ml × 10-3 was 1.169 [95% CI (1.093-1.250), p < 0.001]. In addition, the 28-day cumulative survival rate of the high Cst-EP group was significantly lower than that of the low Cst-EP group. CONCLUSION: EP can be used to predict the severity of ARDS, and Cst-EP is associated with mortality during controlled mechanical ventilation in ARDS.

[Transcriptomics analysis of key genes and signaling pathways in sepsis-related exogenous acute respiratory distress syndrome].

OBJECTIVE: To analyze the differentially expressed gene (DEG) in rats with sepsis-induced exogenous acute respiratory distress syndrome (ARDS) and explore the early diagnosis and protective mechanism of sepsis-induced ARDS at the transcriptome level. METHODS: Twelve 6 to 8 weeks old male Sprague-Dawley (SD) rats were randomly divided into lipopolysaccharide (LPS) induced sepsis-induced ARDS model group (model group, intraperitoneal injection of LPS 15 mg/kg) and control group (intraperitoneal injection of the same volume of normal saline), with 6 rats in each group. RNA was extracted from the left lung tissue of the two groups, and the paired-end sequencing mode of the illumina Hiseq sequencing platform was used for high-throughput sequencing. The DESeq2 software was used to screen DEG with |log2 (fold change, FC)| ≥ 3 and P < 0.001. Gene ontology (GO) function enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed on DEG. STRING and CytoScape software were used to construct a protein-protein interaction (PPI) network and screen key genes. The peripheral blood mononuclear cell (PBMC) of 20 septic patients admitted to the emergency and critical care medical department of Lianyungang First People's Hospital from March to November 2021 and 20 age-matched healthy people in the same period were isolated and extracted, and the key genes were verified by real-time fluorescent quantitative polymerase chain reaction (RT-qPCR). RESULTS: A total of 286 DEG were screened, including 202 up-regulated genes and 84 down-regulated genes. GO enrichment analysis showed that DEG was mainly involved in biological processes such as neutrophil chemotaxis migration, antibacterial humoral response, host immune response, and humoral immune response. KEGG analysis showed that DEG mainly played a biological role through interleukin-17 (IL-17) signaling pathway, tumor necrosis factor (TNF) signaling pathway, and chemokine signaling pathway. In PPI analysis, a total of 262 node proteins were screened, and the interaction relationship was 852 edges. The first 15 key genes were IL-6, TNF, IL-10, IL-1ß, chemokine ligand 1 (CXCL1), CXCL10, chemokine receptor 3 (CXCR3), CXCR2, CXCL9, chemokine ligand 7 (CCL7), CXCL11, CCL1, CXCL13, CCL12, and CCL22. Five representative key genes were performed on PBMC of blood samples from septic ARDS patients and healthy controls by RT-qPCR. The results showed that their expression was significantly higher than that in the healthy controls [IL-6 mRNA (2-ΔΔCt): 2.803±1.081 vs. 0.951±0.359, TNF mRNA (2-ΔΔCt): 2.376±0.799 vs. 1.150±0.504, CXCL10 mRNA (2-ΔΔCt): 2.500±0.815 vs. 1.107±0.515, CXCR3 mRNA (2-ΔΔCt): 1.655±0.628 vs. 0.720±0.388, CCL22 mRNA (2-ΔΔCt): 1.804±0.878 vs. 1.010±0.850, all P < 0.05], and the trends were consistent with the RNA-Seq results. CONCLUSIONS: Biological processes such as chemotactic migration and degranulation of inflammatory cells, cytokine immune response, and signal pathways such as CXCL10/CXCR3 and IL-17 play important roles in the occurrence and development of sepsis-related exogenous ARDS, which would provide new ideas and targets for further study of lung injury mechanisms and clinical prevention and treatment.

Development and validation of a mechanical power-oriented prediction model of weaning failure in mechanically ventilated patients: a retrospective cohort study.

OBJECTIVE: To develop and validate a mechanical power (MP)-oriented prediction model of weaning failure in mechanically ventilated patients. DESIGN: A retrospective cohort study. SETTING: Data were collected from the large US Medical Information Mart for Intensive Care-IV (MIMIC-IV) V.1.0, which integrates comprehensive clinical data from 76 540 intensive care unit (ICU) admissions from 2008 to 2019. PARTICIPANTS: A total of 3695 patients with invasive mechanical ventilation for more than 24 hours and weaned with T-tube ventilation strategies were enrolled from the MIMIC-IV database. PRIMARY AND SECONDARY OUTCOME: Weaning failure. RESULTS: All eligible patients were randomised into development cohorts (n=2586, 70%) and validation cohorts (n=1109, 30%). Multivariate logistic regression analysis of the development cohort showed that positive end-expiratory pressure, dynamic lung compliance, MP, inspired oxygen concentration, length of ICU stay and invasive mechanical ventilation duration were independent predictors of weaning failure. Calibration curves showed good correlation between predicted and observed outcomes. The prediction model showed accurate discrimination in the development and validation cohorts, with area under the receiver operating characteristic curve values of 0.828 (95% CI: 0.812 to 0.844) and 0.833 (95% CI: 0.809 to 0.857), respectively. Decision curve analysis indicated that the predictive model was clinically beneficial. CONCLUSION: The MP-oriented model of weaning failure accurately predicts the risk of weaning failure in mechanical ventilation patients and provides valuable information for clinicians making decisions on weaning.

Whole Transcriptomic Analysis of Key Genes and Signaling Pathways in Endogenous ARDS.

Objective: To analyze the differentially expressed genes (DEGs) in rats with endogenous acute respiratory distress syndrome (ARDS) lung injury and explore the pathogenesis and early diagnostic molecular markers using whole transcriptomic data. Methods: Twelve 8-week-old male Sprague Dawley rats were selected and randomly and equally divided into ARDS lung injury group and normal control group. RNA was extracted from the left lung tissues of both the groups and sequenced using the paired-end sequencing mode of the Illumina Hiseq sequencing platform. The DEGs of miRNA, cirRNA, lncRNA, and mRNA were screened using DESeq2 software, and the ceRNA regulatory network was constructed using Cytoscape. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were performed using the mRNA DEGs. STRING and Cytoscape software were used to construct the protein interaction network and identify the 15 key genes, which were verified using quantitative real-time polymerase chain reaction (qRT-PCR). Results: Based on different screening conditions, and compared with the control group, the ARDS lung injury group showed 836 mRNA DEGs (386 upregulated and 450 downregulated), 110 lncRNA DEGs (53 upregulated and 57 downregulated), 19 circRNA DEGs (3 upregulated and 16 downregulated), and 6 miRNA DEGs (5 upregulated and 1 downregulated gene). GO showed that the DEGs of mRNA were mainly involved in biological processes, such as defense response to lipopolysaccharide and other organisms, leukocyte chemotaxis, neutrophil chemotaxis, and cytokine-mediated signaling. KEGG enrichment analysis showed that the DEGs played their biological roles mainly by participating in IL-17, TNF, and chemokine signaling pathways. The PPI analysis showed a total of 281 node proteins and 634 interaction edges. The top 15 key genes, which were screened, included Cxcl10, Mx1, Irf7, Isg15, Ifit3, Ifit2, Rsad2, Ifi47, Oasl, Dhx58, Usp18, Cmpk2, Herc6, Ifit1, and Gbp4. The ceRNA network analysis showed 69 nodes and 73 correlation pairs, where the key gene nodes were miR-21-3p, Camk2g, and Stx2. Conclusions: The chemotaxis, migration, and degranulation of inflammatory cells, cytokine immune response, autophagy, and apoptosis have significant biological functions in the occurrence and development of endogenous acute lung injury during ARDS. Thus, the camk2g/miR-21-3p/lncRNA/circRNA network, CXCL10/CXCR3, and IL-17 signaling pathways might provide novel insights and targets for further studying the lung injury mechanism and clinical treatment.

Identification and validation of autophagy-related genes in exogenous sepsis-induced acute respiratory distress syndrome.

OBJECTIVE: To analyze the differential expression of autophagy-related genes of sepsis-induced acute respiratory distress syndrome (ARDS) as potential markers for early diagnosis. METHODS: Male Sprague-Dawley rats (aged 8 weeks) were selected and randomly divided into sepsis-induced ARDS group (n = 6) and a normal control group (n = 6). Lung tissue samples were collected for high-throughput sequencing using Illumina HiSeq sequencing platform in the paired-end sequencing mode. Differentially expressed genes (DEGs) were screened by DESeq. 2 software [|log2FC | ≥1 and p < .05] and autophagy-related genes were identified using Mouse Genome Informatics. Co-expressed autophagy-related DEGs from these two datasets were filtered by construction of a Venn diagram. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed on these autophagy-related DEGs and a protein interaction network was constructed using STRING and Cytoscape software to identify hub genes, which were verified by real-time quantitative polymerase chain reaction (qRT-PCR). RESULTS: A total of 42 autophagy-related DEGs (26 upregulated genes and 16 downregulated genes) were identified. The GO and KEGG pathway analyses showed enrichment in 969 biological processes (BPs), three cellular components (CCs), eight molecular functions (MFs) and 27 signaling pathways. The protein interaction (PPI) network revealed 42 node proteins and 75 interacting edges, with an average node degree of 3.52, and an average local clustering coefficient of 0.509. Among the top 10 hub genes with the RNA-Seq, six hub genes (Stat3, Il10, Ifng, Hmox1, Hif1a, and Nod2) were validated by qRT-PCR (all p < .05). CONCLUSION: 42 potential autophagy-related genes associated with sepsis-induced ARDS lung injury were identified and six hub genes (Stat3, Il10, Ifng, Hmox1, Hif1a, and Nod2) may affect the development of ARDS by regulating autophagy. These results expanded our understanding of ARDS and might be useful in treatment of exogenous sepsis-induced ARDS.

Efficacy and Prognosis of Ultrasound-Guided Percutaneous Catheter Drainage in Patients with Liver Abscess Complicated with Septic Shock.

Objective: Currently, the therapeutic effect and outcomes of US-PCD in patients with liver abscess and septic shock remain unclear. This study is aimed at investigating the effects of ultrasound-guided percutaneous catheter drainage (US-PCD) on the prognosis of patients with liver abscess complicated with septic shock. Method: We retrieved and assessed the data of 120 patients with liver abscess complicated with septic shock diagnosed at our hospital from January 2019 to March 2021. The patients underwent US-PCD in the observation group or conventional surgical incision and drainage in the control group. After treatment, we determined the levels of liver function indicators alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBIL), direct bilirubin (DBIL), and alkaline phosphatase (ALP) as well as the levels of inflammatory cytokines IL-6, IL-8, and TNF-α in serum using ELISA on postoperative days 0, 2, 4, and 6. The postoperative body temperature recovery, peripheral white blood cell count recovery, extubation, postoperative length of stay, and complications were recorded, with a 12-month follow-up to calculate their survival rate. Results: After treatment, the ALT, AST, TBIL, DBIL, and ALP levels and inflammatory factor levels in the two groups were gradually reduced over time and returned to the normal range with a better recovery trend in the observation group. US-PCD was associated with better postoperative body temperature recovery, peripheral white blood cell count recovery, shorter extubation time, hospital stay, lower postoperative rate, and a higher survival rate. Conclusion: US-PCD may be effective in treating liver abscess and can significantly improve the prognosis of patients.

[Critical coronavirus disease 2019 complicated with heparin resistance in 2 patients].

OBJECTIVE: To explore the diagnosis process and treatment experience of severe coronavirus disease 2019 (COVID-19) patients with heparin resistance (HR). METHODS: The medical team of the First People's Hospital of Lianyungang admitted 2 severe COVID-19 patients with HR in intensive care unit (ICU) during their support to the designated hospital for the treatment of COVID-19 patients in Lianyungang City in November 2021. The clinical features, laboratory examinations, imaging features, treatment and prognosis of the two patients were analyzed. RESULTS: Both severe COVID-19 patients received mechanical ventilation, 1 patient was treated with extracorporeal membrane oxygenation (ECMO) support. Both patients were complicated with lower extremity deep venous thrombosis and HR phenomenon under routine dose anticoagulant therapy. The maximum daily dose of unfractionated heparin exceeded 35 000 U (up to 43 200 U), the 2 patients failed to meet the standard of anticoagulation treatment, and the course of disease was prolonged. After that, argatroban was given 0.4 µg×kg-1×min-1 combined with anticoagulant therapy, the activated partial thromboplastin time (APTT) of patients undergoing ECMO could be maintained at 55-60 seconds and the activated coagulation time (ACT) of them could be maintained at 180-200 seconds. After ECMO support or later sequential mechanical ventilation, both patients recovered and were discharged, and deep venous thrombosis was also effectively controlled. CONCLUSIONS: HR phenomenon often occurs during the treatment of severe COVID-19 patients, the anticoagulation regimen should be adjusted in time, and the anticoagulation effect combined with argatroban is clear.

Acute reduction of erector spinae muscle cross-sectional area is associated with ICU-AW and worse prognosis in patients with mechanical ventilation in the ICU: A prospective observational study.

BACKGROUND: To investigate the values of erector spinae muscle cross-sectional area (ESMcsa) loss for diagnosing intensive care unit-acquired weakness (ICU-AW) and predicting the 60-day survival status in patients with mechanical ventilation. METHODS: Patients who were admitted into the intensive care unit (ICU) and received invasive mechanical ventilation therapy from June 2018 to June 2020 were selected. And they were divided into an ICU-AW group and a non-ICU-AW group, which were compared based on the ESMcsa and The British Medical Research Council muscle strength score (MRC-score) on the 1st and 7th day of ICU admission. The receiver operating characteristic curve was employed to measure the values of the ESMcsa Loss and ESMcsa Loss Ratio on the 7th day in order to diagnose ICU-AW in patients with mechanical ventilation. The survival curves of the patients were plotted to analyze the ESMcsa Loss Ratio values for predicting the 60-day survival status. RESULTS: A total of 104 patients were enrolled, they were divided into the ICU-AW group (n = 56) and the non-ICU-AW group (n = 48). The mechanical ventilation time, ICU stay time, and hospital stay time of the ICU-AW group were all significantly higher than those of the non-ICU-AW group. On the 1st day, no significant difference in the ESMcsa or MRC-score between the 2 groups of patients was observed. On the 7th day, the ESMcsa and MRC-score of the ICU-AW group were significantly lower than those of the non-ICU-AW group. The ESMcsa Loss and ESMcsa Loss Ratio were both significantly negatively correlated with the MRC-score. The ESMcsa Loss and ESMcsa Loss Ratio on the 7th day were both valuable for the prediction of ICU-AW in patients with mechanical ventilation (areas under the receiver operating characteristic curve = 0.904, 0.835, and 0.889, P < .001). The survival rate of the patients in the high- and low-ESMcsa Loss Ratio groups were 60.0% and 80.0% (P < .05). CONCLUSIONS: As suggested by the ESMcsa Loss Ratios of the patients with mechanical ventilation on the 7th day of ICU admission, it offers a desirable objective indicator for the diagnosis of ICU-AW, and provides certain values for predicting the 60-day survival status of patients with mechanical ventilation in the ICU.

AKR1C1 alleviates LPS­induced ALI in mice by activating the JAK2/STAT3 signaling pathway.

Acute lung injury (ALI) is a respiratory tract disease characterized by increased alveolar/capillary permeability, lung inflammation and structural damage to lung tissues, which can progress and transform into acute respiratory distress syndrome (ARDS). Although there are several treatment strategies available to manage this condition, there is still no specific cure for ALI. Aldo­keto reductase family 1 member C1 (AKR1C1) is a member of the aldo­keto reductase superfamily, and is a well­known Nrf2 target gene and an oxidative stress gene. The aim of the present study was to investigate the effects of AKR1C1 on a lipopolysaccharide (LPS)­induced ALI model. After mice received LPS treatment, the mRNA expression levels of AKR1C1 in the bronchoalveolar lavage fluid and serum were measured using reverse transcription­quantitative PCR and its relationship with the inflammatory factors and malondialdehyde levels were determined using correlation analysis. Next, AKR1C1 was overexpressed or knocked out in mice, and subsequently ALI was induced in mice using LPS. The severity of ALI, oxidative stress and inflammation in the lungs were measured, and the potential involvement of the Janus kinase 2 (JAK2)/signal transduction activator of transcription 3 (STAT3) signaling pathway was assessed by measuring the changes of lung injury parameters after the agonists of JAK2/STAT3 pathway, including interleukin (IL)­6 and colivelin, were administrated to mice. The results revealed that AKR1C1 expression was decreased in the LPS­induced ALI mouse model. AKR1C1 expression was inversely correlated with serum tumor necrosis factor­α, IL­6 and malondialdehyde levels, and positively correlated with serum IL­10 levels. AKR1C1 overexpression significantly attenuated lung injury, as shown by the changes in Evans blue leakage in the lung, lung wet/dry weight ratio, PaO2/FIO2 ratio, survival rate of mice and histological lung changes. In addition, the JAK2/STAT3 signaling pathway was significantly deactivated by AKR1C1+/+. When AKR1C1+/+ mice were treated with JAK2/STAT3 agonists, the effects of AKR1C1 overexpression on lung injury and oxidative stress were abolished. In conclusion, AKR1C1 may protect against oxidative stress and serve as a negative regulator of inflammation in ALI/ARDS. In addition, the JAK2/STAT3 signaling pathway could participate in the protective effects of AKR1C1 against ALI.

A quantitative model to understand the microflow-controlled sintering mechanism of metal particles at nanometer to micron scale.

In this paper, the particle size effect on the sintering behaviors of Cu particles at nanometer to micron scale is explored. The results show that micron-sized particles could form obvious sintering necks at a low temperature of 260 °C, exhibiting a shear strength as high as 64 MPa. A power relation ofx âˆ a0.8between sintering neck radius (x) and particle radius (a) is discovered, and a sintering model with a quantitative relational expression of (x/a)5 = 160γδDt/3akTis proposed by considering the surface tension driven microflow process between adjacent particles to predict the growth of sintering necks. It is concluded that the sintering process of particles at nanometer to micron scale is controlled by microflow mechanism instead of diffusion mechanism. Our proposed model provides a new theoretical basis for understanding the kinetic growth mechanism of sintering necks of metal particles.

Manipulating Carrier Concentration by Self-Assembled Monolayers in Thermoelectric Polymer Thin Films.

Conjugated polymers have attracted considerable attention for thermoelectric applications in recent years due to their plentiful resources, diverse structures, mechanical flexibility, and low thermal conductivity. Herein, we demonstrate a new strategy of modulating charge carrier concentration of chemical-doped polymer films by modifying the substrate with self-assembled monolayers (SAMs). The SAM with a trifluoromethyl terminal group is found to accumulate holes in the polymer thin films, while the SAM with an amino terminal group tends to donate electrons to the polymer films. Thermoelectric thin films of conjugated donor-acceptor copolymer exhibit high power factors of 55.6-61.0 µW m-1 K-2 on SAMs with polar terminal groups. These power factors are 49% higher than that on the SAM with the nonpolar terminal group and 3 times higher than that on pristine substrate. The high power factor is ascribed to the modulated charge carrier concentration and improved charge carrier mobility as induced by SAMs.

Electroless deposition of Ni-P/Au coating on Cu substrate with improved corrosion resistance from Au(iii)-DMH based cyanide-free plating bath using hypophosphite as a reducing agent.

The green cyanide-free gold deposition is an important development direction in electroless gold plating. However, the commonly Au(i) based cyanide-free gold plating bath always suffers from severe corrosion to the Ni-P layer and unsatisfactory service life of the bath. In this work, a green and environmentally friendly cyanide-free gold plating bath was developed with hypophosphite added as a reducing agent into the Au(iii)-DMH (5,5-dimethylhydantoin) based plating bath to retard the corrosion of the Ni-P layer. SEM micrographs combined with XRD and XPS analysis indicated that the electroless deposited gold was pure and compact. And XRD also revealed that the oriented deposition of gold was growing preferentially on Au (111). Corrosion tests, including salt spray tests, potentiodynamic polarization tests, and electrochemical impedance spectroscopy tests, indicated that the obtained Cu/Ni-P/Au coatings had significantly improved corrosion resistance performance with the loading of hypophosphite as the reducing agent. The baths remained transparent and no turbidity or precipitates were detected for 210 days, reflecting good stability. The detection for the Ni2+ concentration in the bath showed that adding hypophosphite could retard the replacement reaction between Au3+ and the Ni-P layer in part and this is important for decreasing the severe corrosion of the Ni-P layer. Moreover, Au was inactive for catalyzing the oxidation of hypophosphite during the deposition process which was confirmed furthermore via quantum chemical calculations. Therefore, our developed green cyanide-free electroless gold deposition process can beneficially provide research value and application prospects in microelectronic industry.

Conductive Metal-Organic Frameworks: Mechanisms, Design Strategies and Recent Advances.

Metal-organic frameworks (MOFs), constructed from metal ions and organic ligands through coordination assembly, exhibit considerable conductivity, which originates from the ionic or electronic transport pathway between the host architecture and guest species. In recent decades, the study of conductive MOFs has accelerated deservedly due to their importance in the electronic information industry. In this review, we first briefly describe the different mechanisms of ionic and electronic conduction. The design strategies of constructing intrinsic and doping MOFs are then summarized and generalized into three major categories (host-based-, guest-based- and host-guest-related systems) in terms of promoting conductive performance. In the next section we provide an overview of recent progress in research on conductive MOFs, providing details according to the various carriers of transporting electrons, protons and other ions. We conclude with a discussion on the practicability and emerging applications of conductive MOFs and a section on the existing challenges and development prospects. Conduction mechanisms, design strategies, recent progresses and emerging applications of conductive MOFs.

Experimental and DFT study of the effect of mercaptosuccinic acid on cyanide-free immersion gold deposition.

In order to search for an effective alternative to cyanide for gold plating, mercaptosuccinic acid (MSA) was selected as the complexing agent of Au+ by open circuit potential tests and gold plating compared with 1-hydroxyethylidene-1,1-diphosphonic acid and aminomethylphosphonic acid. For the first time, a novel, stable, slightly acidic and cyanide-free gold plating bath was prepared. Scanning electron microscopy, Tafel tests, and tin dipping tests showed that the Cu/Ni-P/Au coating had a fine and even grain size, no black pad, good corrosion resistance, and good weldability. Quantum chemical calculations based on density functional theory were used to further study complexants and complexes. Molecular electrostatic potential indicates that Au+ approaches MSA in the direction of C[double bond, length as m-dash]O. Frontier molecular orbital theory, atomic contribution to orbital composition, condensed local softness, and average local ionization energy indicate that the coordination capacity of the S atom in MSA is much stronger than that of other atoms. Fuzzy bond order analysis shows that the S-Au-S coordination structure is the most stable form in the plating solution. UV-visible absorption spectroscopy clarifies that the wavelength is redshifted when MSA-Au(i) ions form.

Identification of DDX58 and CXCL10 as Potential Biomarkers in Acute Respiratory Distress Syndrome.

Acute respiratory distress syndrome (ARDS) is a devastating condition of acute inflammatory lung injury and causes high morbidity and mortality. Therefore, investigations on the effective biomarkers will be significant for the understanding of ARDS. In our research, the gene expression profiles of 27 samples from ARDS patients (n = 18) and healthy controls (n = 9) were analyzed and eight gene co-expression modules were identified by constructing weighted gene co-expression network. The correlation analysis of modules with phenotypes showed that genes in the yellow and black modules, which were significantly enriched in the ARDS-related pathways, such as TNF signaling pathway, Toll-like receptor signaling pathway, and NF-kappa B signaling pathway, were associated with the phenotype "time postinfection." Genes DDX58 and CXCL10, which were highly expressed after infection and significantly enriched in ARDS-related pathways, presented high score in protein-protein interaction analysis, indicating that they may be associated with ARDS and providing novel biomarkers for its diagnosis, treatment, and surveillance.

A Dipleiadiene-Embedded Aromatic Saddle Consisting of 86 Carbon Atoms.

This study presents a new type of negatively curved nanographene (C86 H32 ) that contains an unprecedented pattern of heptagons. A tert-butylated derivative of C86 H32 was successfully synthesized using tetrabenzodipleiadiene as a key building block. This synthesis involved a ring expansion reaction as a key step to form the seven-membered rings in the framework of tetrabenzodipleiadiene. The single-crystal structure reveals a saddle-shaped molecule with a highly bent naphthalene moiety at the center of the polycyclic backbone. As found from the DFT calculations, this aromatic saddle is flexible at room temperature and has a saddle-shaped geometry as the dominant conformation. The DFT calculations along with experimental results show that the attachment of t-butyl groups to the central tetrabenzodipleiadiene moiety of nanographene C86 H32 can stabilize the saddle conformation and make this nanographene less flexible.