Wnt5a-mediated autophagy contributes to the epithelial-mesenchymal transition of human bronchial epithelial cells during asthma.

BACKGROUND: The epithelial-mesenchymal transition (EMT) of human bronchial epithelial cells (HBECs) is essential for airway remodeling during asthma. Wnt5a has been implicated in various lung diseases, while its role in the EMT of HBECs during asthma is yet to be determined. This study sought to define whether Wnt5a initiated EMT, leading to airway remodeling through the induction of autophagy in HBECs. METHODS: Microarray analysis was used to investigate the expression change of WNT5A in asthma patients. In parallel, EMT models were induced using 16HBE cells by exposing them to house dust mites (HDM) or interleukin-4 (IL-4), and then the expression of Wnt5a was observed. Using in vitro gain- and loss-of-function approaches via Wnt5a mimic peptide FOXY5 and Wnt5a inhibitor BOX5, the alterations in the expression of the epithelial marker E-cadherin and the mesenchymal marker protein were observed. Mechanistically, the Ca2+/CaMKII signaling pathway and autophagy were evaluated. An autophagy inhibitor 3-MA was used to examine Wnt5a in the regulation of autophagy during EMT. Furthermore, we used a CaMKII inhibitor KN-93 to determine whether Wnt5a induced autophagy overactivation and EMT via the Ca2+/CaMKII signaling pathway. RESULTS: Asthma patients exhibited a significant increase in the gene expression of WNT5A compared to the healthy control. Upon HDM and IL-4 treatments, we observed that Wnt5a gene and protein expression levels were significantly increased in 16HBE cells. Interestingly, Wnt5a mimic peptide FOXY5 significantly inhibited E-cadherin and upregulated α-SMA, Collagen I, and autophagy marker proteins (Beclin1 and LC3-II). Rhodamine-phalloidin staining showed that FOXY5 resulted in a rearrangement of the cytoskeleton and an increase in the quantity of stress fibers in 16HBE cells. Importantly, blocking Wnt5a with BOX5 significantly inhibited autophagy and EMT induced by IL-4 in 16HBE cells. Mechanistically, autophagy inhibitor 3-MA and CaMKII inhibitor KN-93 reduced the EMT of 16HBE cells caused by FOXY5, as well as the increase in stress fibers, cell adhesion, and autophagy. CONCLUSION: This study illustrates a new link in the Wnt5a-Ca2+/CaMKII-autophagy axis to triggering airway remodeling. Our findings may provide novel strategies for the treatment of EMT-related diseases.

CGRP is essential for protection against alveolar epithelial cell necroptosis by activating the AMPK/L-OPA1 signaling pathway during acute lung injury.

Alveolar epithelial cell (AEC) necroptosis is critical to disrupt the alveolar barrier and provoke acute lung injury (ALI). Here, we define calcitonin gene-related peptide (CGRP), the most abundant endogenous neuropeptide in the lung, as a novel modulator of AEC necroptosis in lipopolysaccharide (LPS)-induced ALI. Upon LPS-induced ALI, overexpression of Cgrp significantly mitigates the inflammatory response, alleviates lung tissue damage, and decreases AEC necroptosis. Similarly, CGRP alleviated AEC necroptosis under the LPS challenge in vitro. Previously, we identified that long optic atrophy 1 (L-OPA1) deficiency mediates mitochondrial fragmentation, leading to AEC necroptosis. In this study, we discovered that CGRP positively regulated mitochondrial fusion through stabilizing L-OPA1. Mechanistically, we elucidate that CGRP activates AMP-activated protein kinase (AMPK). Furthermore, the blockade of AMPK compromised the protective effect of CGRP against AEC necroptosis following the LPS challenge. Our study suggests that CRGP-mediated activation of the AMPK/L-OPA1 axis may have potent therapeutic benefits for patients with ALI or other diseases with necroptosis.

The Role of Mitochondrial Quality Control in Chronic Obstructive Pulmonary Disease.

Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity, mortality, and health care use worldwide with heterogeneous pathogenesis. Mitochondria, the powerhouses of cells responsible for oxidative phosphorylation and energy production, play essential roles in intracellular material metabolism, natural immunity, and cell death regulation. Therefore, it is crucial to address the urgent need for fine-tuning the regulation of mitochondrial quality to combat COPD effectively. Mitochondrial quality control (MQC) mainly refers to the selective removal of damaged or aging mitochondria and the generation of new mitochondria, which involves mitochondrial biogenesis, mitochondrial dynamics, mitophagy, etc. Mounting evidence suggests that mitochondrial dysfunction is a crucial contributor to the development and progression of COPD. This article mainly reviews the effects of MQC on COPD as well as their specific regulatory mechanisms. Finally, the therapeutic approaches of COPD via MQC are also illustrated.

Evaluation of different scoring systems in the prediction of complications, morbidity, and mortality after laparoscopic radical gastrectomy.

BACKGROUND: This retrospective study aimed to assess the suitability of POSSUM and its modified versions, E-PASS and its modified score, SRS, and SORT scores for predicting postoperative complications and mortality in patients undergoing laparoscopic radical gastrectomy for gastric cancer. MATERIALS AND METHODS: Data analysis was performed on 349 patients who underwent laparoscopic radical gastrectomy at Tianjin Medical University General Hospital between January 2016 and December 2021. The discriminative ability of the scoring systems was evaluated using the area under the receiver operating characteristic curve (AUC). The primary endpoint focused on the prediction of postoperative complications, while the secondary endpoint assessed the prediction of postoperative mortality. RESULTS: Among the scoring systems evaluated, the modified E-PASS (mE-PASS) score exhibited the highest AUC (0.846) and demonstrated the highest sensitivity (81%) and specificity (79%) for predicting postoperative complications. All other scores, except for POSSUM, showed moderate discriminative ability in predicting complications. In terms of predicting postoperative mortality, the E-PASS score had the highest AUC (0.978), while the mE-PASS score displayed the highest sensitivity (76%) and specificity (90%). Notably, both E-PASS and mE-PASS scores exhibited excellent discriminative ability. CONCLUSIONS: The P-POSSUM, O-POSSUM, E-PASS, mE-PASS, SRS, and SORT scoring systems are useful tools for predicting postoperative outcomes in laparoscopic radical gastrectomy. Among them, the mE-PASS score demonstrated the best predictive power. However, the POSSUM system could only be applicable to predict postoperative mortality.

EETs alleviate alveolar epithelial cell senescence by inhibiting endoplasmic reticulum stress through the Trim25/Keap1/Nrf2 axis.

Alveolar epithelial cell (AEC) senescence is a key driver of a variety of chronic lung diseases. It remains a challenge how to alleviate AEC senescence and mitigate disease progression. Our study identified a critical role of epoxyeicosatrienoic acids (EETs), downstream metabolites of arachidonic acid (ARA) by cytochrome p450 (CYP), in alleviating AEC senescence. In vitro, we found that 14,15-EET content was significantly decreased in senescent AECs. Exogenous EETs supplementation, overexpression of CYP2J2, or inhibition of EETs degrading enzyme soluble epoxide hydrolase (sEH) to increase EETs alleviated AECs' senescence. Mechanistically, 14,15-EET promoted the expression of Trim25 to ubiquitinate and degrade Keap1 and promoted Nrf2 to enter the nucleus to exert an anti-oxidant effect, thereby inhibiting endoplasmic reticulum stress (ERS) and alleviating AEC senescence. Furthermore, in D-galactose (D-gal)-induced premature aging mouse model, inhibiting the degradation of EETs by Trifluoromethoxyphenyl propionylpiperidin urea (TPPU, an inhibitor of sEH) significantly inhibited the protein expression of p16, p21, and γH2AX. Meanwhile, TPPU reduced the degree of age-related pulmonary fibrosis in mice. Our study has confirmed that EETs are novel anti-senescence substances for AECs, providing new targets for the treatment of chronic lung diseases.

Mitochondrial citrate accumulation drives alveolar epithelial cell necroptosis in lipopolysaccharide-induced acute lung injury.

Necroptosis is the major cause of death in alveolar epithelial cells (AECs) during acute lung injury (ALI). Here, we report a previously unrecognized mechanism for necroptosis. We found an accumulation of mitochondrial citrate (citratemt) in lipopolysaccharide (LPS)-treated AECs because of the downregulation of Idh3α and citrate carrier (CIC, also known as Slc25a1). shRNA- or inhibitor-mediated inhibition of Idh3α and Slc25a1 induced citratemt accumulation and necroptosis in vitro. Mice with AEC-specific Idh3α and Slc25a1 deficiency exhibited exacerbated lung injury and AEC necroptosis. Interestingly, the overexpression of Idh3α and Slc25a1 decreased citratemt levels and rescued AECs from necroptosis. Mechanistically, citratemt accumulation induced mitochondrial fission and excessive mitophagy in AECs. Furthermore, citratemt directly interacted with FUN14 domain-containing protein 1 (FUNDC1) and promoted the interaction of FUNDC1 with dynamin-related protein 1 (DRP1), leading to excessive mitophagy-mediated necroptosis and thereby initiating and promoting ALI. Importantly, necroptosis induced by citratemt accumulation was inhibited in FUNDC1-knockout AECs. We show that citratemt accumulation is a novel target for protection against ALI involving necroptosis.

TREM-1 exacerbates bleomycin-induced pulmonary fibrosis by aggravating alveolar epithelial cell senescence in mice.

Our previous study showed that triggering receptors expressed on myeloid cell-1 (TREM-1) was upregulated in bleomycin (BLM)-induced pulmonary fibrosis (PF) mouse model. However, the role of TREM-1 in the development of PF and its underlying mechanism remain unclear. Herein, we report that the prophylactical blockade of TREM-1 using a decoy peptide dodecapeptide (LR12) exerted protective effects against BLM-induced PF in mice, with a higher survival rate, attenuated tissue injury, and less extracellular matrix deposition. Interestingly, therapeutic blockade of TREM-1 at the early stage of fibrosis also attenuated BLM-induced PF, suggesting a non-inflammatory effect. More importantly, we observed that TREM-1 blockade with LR12 significantly reduced the expression of the senescence-relative protein, including p16, p21, p53, and γ-H2AX in the lungs of PF mice. Notably, TREM-1 was upregulated in alveolar epithelial cells (AECs) and correlated with the levels of senescence markers in BLM-treated mice. In vitro, activating TREM-1 with an agonistic antibody exacerbated BLM-induced senescence in MLE12 cells, a murine AEC cell line. Furthermore, prophylactic or therapeutic blockade of TREM-1 protected MLE12 cells from senescence induced by BLM or H2O2. In conclusion, our findings elucidate a pro-fibrotic effect of TREM-1 by inducing AECs senescence in PF, providing a potential strategy for fibrotic disease treatment.

Epoxyeicosatrienoic Acids Inhibit the Activation of Murine Fibroblasts by Blocking the TGF-ß1-Smad2/3 Signaling in a PPARγ-Dependent Manner.

Background: Epoxyeicosatrienoic acids (EETs), the metabolite of arachidonic acid by cytochrome P450 (CYP), reportedly serve as a vital endogenous protective factor in several chronic diseases. EETs are metabolized by soluble epoxide hydrolase (sEH). We have observed that prophylactic blocking sEH alleviates bleomycin- (BLM-) induced pulmonary fibrosis (PF) in mice. However, the underlying mechanism and therapeutic effects of EETs on PF remain elusive. Objective: In this study, we investigated the effect of CYP2J2/EETs on the activation of murine fibroblasts and their mechanisms. Results: we found that administration of the sEH inhibitor (TPPU) 7 days after the BLM injection also reversed the morphology changes and collagen deposition in the lungs of BLM-treated mice, attenuating PF. Fibroblast activation is regarded as a critical role of PF. Therefore, we investigated the effects of EETs on the proliferation and differentiation of murine fibroblasts. Results showed that the overexpression of CYP2J2 reduced the cell proliferation and the expressions of α-SMA and PCNA induced by transforming growth factor- (TGF-) ß1 in murine fibroblasts. Then, we found that EETs inhibited the proliferation and differentiation of TGF-ß1-treated-NIH3T3 cells and primary murine fibroblasts. Mechanistically, we found that 14,15-EET disrupted the phosphorylation of Smad2/3 murine fibroblasts by activating PPARγ, which was completely abolished by a PPARγ inhibitor GW9662. Conclusion: our study shows that EETs inhibit the activation of murine fibroblasts by blocking the TGF-ß1-Smad2/3 signaling in a PPARγ-dependent manner. Regulating CYP2J2-EET-sEH metabolic pathway may be a potential therapeutic option in PF.

LIMK1: A promising prognostic and immune infiltration indicator in colorectal cancer.

Studies have shown that LIM domain kinase 1 (LIMK1) is upregulated in a variety of tumors and may be a potential detection target. The present study analyzed the expression difference of LIMK1 and its relationship with tumor clinicopathological characteristics and tumor microenvironment in colorectal cancer (CRC). The transcriptomic data of LIMK1 with CRC were downloaded from The Cancer Genome Atlas (TCGA) database and GEO databases for analyzing the expression of LIMK1 mRNA and the correlation with the prognosis of patients. The protein expression of LIMK1 was obtained from the Human Protein Atlas. The receiver operating characteristic (ROC) curve and Kaplan-Meier was used to evaluate the expression characteristics and prognostic differences of LIMK1 in CRC. STRING was used to analyze co-expression genes of LIMK1. The tumor immune estimation resource was applied to the correlation between LIMK1 expression and immune infiltrates. The present study verified LIMK1 expression at the level of clinical samples collected from the Tianjin Medical University General Hospital and cell lines using reverse transcription-quantitative PCR. The mRNA and protein expression of LIMK1 were both upregulated in tumor tissues compared with adjacent tissues in CRC. The expression levels of LIMK1 were positively associated with clinical-pathological features of CRC including lymphatic invasion (P=4.00×10-2) and high pathologic stages (P=4.20×10-2). The AUC value of LIMK1 in CRC was 0.937 (95% CI: 0.918-0.957) through ROC analysis. Under the best cut-off value (4.009), the sensitivity and specificity were 98 and 81.9%. LIMK1 expression was mainly related to CD4+ T cells, macrophages and dendritic cells in the immune microenvironment of CRC. In conclusion, the high expression of LIMK1 in CRC was closely related to the clinical features and prognosis of patients. Therefore, LIMK1 was a promising prognostic indicator and a potential target for immunotherapy in CRC.

COX-2/sEH Dual Inhibitor PTUPB Attenuates Epithelial-Mesenchymal Transformation of Alveolar Epithelial Cells via Nrf2-Mediated Inhibition of TGF-ß1/Smad Signaling.

Background: Arachidonic acid (ARA) metabolites are involved in the pathogenesis of epithelial-mesenchymal transformation (EMT). However, the role of ARA metabolism in the progression of EMT during pulmonary fibrosis (PF) has not been fully elucidated. The purpose of this study was to investigate the role of cytochrome P450 oxidase (CYP)/soluble epoxide hydrolase (sEH) and cyclooxygenase-2 (COX-2) metabolic disorders of ARA in EMT during PF. Methods: A signal intratracheal injection of bleomycin (BLM) was given to induce PF in C57BL/6 J mice. A COX-2/sEH dual inhibitor PTUPB was used to establish the function of CYPs/COX-2 dysregulation to EMT in PF mice. In vitro experiments, murine alveolar epithelial cells (MLE12) and human alveolar epithelial cells (A549) were used to explore the roles and mechanisms of PTUPB on transforming growth factor (TGF)-ß1-induced EMT. Results: PTUPB treatment reversed the increase of mesenchymal marker molecule α-smooth muscle actin (α-SMA) and the loss of epithelial marker molecule E-cadherin in lung tissue of PF mice. In vitro, COX-2 and sEH protein levels were increased in TGF-ß1-treated alveolar epithelial cells (AECs). PTUPB decreased the expression of α-SMA and restored the expression of E-cadherin in TGF-ß1-treated AECs, accompanied by reduced migration and collagen synthesis. Moreover, PTUPB attenuated TGF-ß1-Smad2/3 pathway activation in AECs via Nrf2 antioxidant cascade. Conclusion: PTUPB inhibits EMT in AECs via Nrf2-mediated inhibition of the TGF-ß1-Smad2/3 pathway, which holds great promise for the clinical treatment of PF.

L-OPA1 deficiency aggravates necroptosis of alveolar epithelial cells through impairing mitochondrial function during acute lung injury in mice.

Necroptosis, a recently described form of programmed cell death, is the main way of alveolar epithelial cells (AECs) death in acute lung injury (ALI). While the mechanism of how to trigger necroptosis in AECs during ALI has been rarely evaluated. Long optic atrophy protein 1 (L-OPA1) is a crucial mitochondrial inner membrane fusion protein, and its deficiency impairs mitochondrial function. This study aimed to investigate the role of L-OPA1 deficiency-mediated mitochondrial dysfunction in AECs necroptosis. We comprehensively investigated the detailed contribution and molecular mechanism of L-OPA1 deficiency in AECs necroptosis by inhibiting or activating L-OPA1. First, our data showed that L-OPA1 expression was downregulated in the lungs and AECs under the lipopolysaccharide (LPS) challenge. Furthermore, inhibition of L-OPA1 aggravated the pathological injury, inflammatory response, and necroptosis in the lungs of LPS-induced ALI mice. In vitro, inhibition of L-OPA1 induced necroptosis of AECs, while activation of L-OPA1 alleviated necroptosis of AECs under the LPS challenge. Mechanistically, inhibition of L-OPA1 aggravated necroptosis of AECs by inducing mitochondrial fragmentation and reducing mitochondrial membrane potential. While activation of L-OPA1 had the opposite effects. In summary, these findings indicate for the first time that L-OPA1 deficiency mediates mitochondrial fragmentation, induces necroptosis of AECs, and exacerbates ALI in mice.

Optimal Reconstruction After Laparoscopic Distal Gastrectomy: A Single-Center Retrospective Study.

OBJECTIVES: Although laparoscopic distal gastrectomy has been widely used for distal gastric cancer, the best functional reconstruction type has not yet been established. Based on previous experience, we propose a modified uncut Roux-en-Y anastomosis. This study aimed to compare the outcomes of different intracorporeal anastomoses after laparoscopic distal gastrectomy. METHODS: From April 2015 to August 2020, the data of 215 patients who underwent laparoscopic distal gastrectomy was collected. The patients were divided into 4 groups according to the digestive tract reconstruction method, Billroth-I, Billroth-II, Roux-en-Y, and the modified uncut Roux-en-Y. Clinicopathologic characteristics, surgery details, short-term outcomes, and postoperative nutritional status were analyzed. RESULTS: The operation time of Billroth-I anastomosis was significantly shorter (216.2 ± 25.8 min, P < .001) than that of other methods. There was no difference in postoperative complications and OS among the 4 reconstruction methods. The incidences of esophagitis, gastritis, and bile reflux were significantly lower in the Roux-en-Y and uncut Roux-en-Y group (P < .001) 1 year after surgery. And the postoperative albumin and PNI levels in uncut Roux-en-Y group were higher than those in other groups(P < .05). On multivariate analysis, age and reconstruction type were independently related to esophagitis, gastritis, and bile reflux. Serum albumin and the prognostic nutritional index were significantly higher in the uncut Roux-en-Y group than other groups (P < .05). CONCLUSIONS: All 4 reconstruction techniques are feasible and safe. The Roux-en-Y and uncut Roux-en-Y are superior to Billroth-Ⅰ and Billroth-Ⅱ+Braun in terms of reflux esophagitis, gastritis, and bile reflux. Uncut Roux-en-Y may result in better PNI than the others.

Extracellular citrate serves as a DAMP to activate macrophages and promote LPS-induced lung injury in mice.

Citrate has a prominent role as a substrate in cellular energy metabolism. Recently, citrate has been shown to drive inflammation. However, the role of citrate in lipopolysaccharide (LPS)-induced acute lung injury (ALI) remains unclear. Here, we aimed to clarify whether extracellular citrate aggravated the LPS-induced ALI and the potential mechanism. Our findings demonstrated that extracellular citrate aggravated the pathological lung injury induced by LPS in mice, characterized by up-regulation of pro-inflammatory factors and over-activation of NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome in the lungs. In vitro, we found that citrate treatment significantly augmented the expression of NLRP3 and pro-IL-1ß and enhanced the translocation of NF-κB/p65 into the nucleus. Furthermore, extracellular citrate plus adenosine-triphosphate (ATP) significantly increased the production of reactive oxygen species (ROS) in primary murine macrophages. Inhibiting the production of ROS with a ROS scavenger N-acetyl-L-cysteine (NAC) attenuated the activation of NLRP3 inflammasome. Altogether, we conclude that extracellular citrate may serve as a damage-associated molecular pattern (DAMP) and aggravates LPS-induced ALI by activating the NLRP3 inflammasome.

Template-assisted synthesis of uniform nanosheet-assembled silver hollow microcubes.

Uniform silver hollow microcubes assembled by nanosheets have been synthesized by using Cu(2)O cubes as chemical template at room temperature. In the reaction system, the Ag(+) ions were reduced by Cu(+) ions released from Cu(2)O cubes, meanwhile the morphology of silver growth units were controlled by trisodium citrate in the form of nanosheets around the template during the reaction. It was found that the concentrations of acid, citrate ions and AgNO(3) were critical to the formation of perfect nanosheet-assembled hollow microcubes. According to the experiment results, an interface redox growth mechanism of nanosheet-assembled Ag hollow microcubes was proposed. Since the obtained Ag hollow cubes are composed of Ag nanosheets, the hierarchical shells are bestrewed with pores or gaps which created abundant active "hot spots" for highly sensitive surface enhanced Raman scattering (SERS) detection. The SERS experiments using rhodamine 6G (R6G) as probing molecules showed that the pack density and porous structure of the shell in the final products strongly affected the SERS signals. The product with higher porous shell structure exhibited stronger SERS signals than others, indicating the rough Ag hollow microcubes could act as excellent substrates for ultrasensitive detection.

Synthesis of high saturation magnetization superparamagnetic Fe3O4 hollow microspheres for swift chromium removal.

High saturation magnetization monodisperse Fe(3)O(4) hollow microspheres (109.48 emu/g) with superparamagnetic property at room temperature are promptly synthesized by a one-step solvothermal process with the presence of sodium dodecylbenzenesulfonate as an additive. The as-synthesized products possess superparamagnetism, large cavity, high water solubility, and saturation magnetization at room temperature. In particular, these hollow microspheres exhibit both of a rather short separation time from industry wastewater and a high adsorption capacity about 180 mg/g at high Cr(VI) concentrations, which is much better than those of reported magnetite solid nanoparticles. In addition, the X-ray photoelectron spectra (XPS) show that the uptake of Cr(VI) into the spheres was mainly governed by a physicochemical process. The micelle-assisted Ostwald ripening process was proposed to explain the rapid formation of hollow structures by a series of control experiments. The as-manufactured products with the two advantages mentioned above serve as ideal candidates for environmental remediation materials.

In vivo evaluation of a new surfactant polymer coating mimicking the glycocalyx of endothelial cells.

The purpose of this study was to demonstrate that a proprietary surfactant polymer (SP) coating does not adversely affect the hemodynamic performance of cardiopulmonary bypass (CPB) or gas exchange in oxygenators. The new coating was applied to a CPB circuit including cannulae, reservoir, oxygenator, and blood pump implanted into 12 pigs, divided into groups with either coated or noncoated pumps. CPB flow was maintained at a fixed level of approximately 2.4 L/min for 6 hours with full heparinization. Hemodynamic data and pump performance were recorded every hour, and blood samples were taken every 2 hours. After sacrifice, the CPB circuit and major organs were macroscopically examined. There was no significant difference in the oxygen transfer rate between the two groups. The coating did not adversely affect oxygenator inlet or outlet pressures. There was no significant difference between the two groups in microthrombi seen in the oxygenators. No thromboemboli were noted in the major organs on gross or histologic examination. In conclusion, this new SP coating did not decrease gas exchange performance, and its biocompatibility evaluations revealed no differences between coated and noncoated groups under aggressive heparin use.

Pd nanoparticle aging and its implications in the suzuki cross-coupling reaction.

Examination of the catalysts recovered in the N,N-dihexylcarbodiimide-palladium nanoparticle composite catalyzed Suzuki cross-coupling reactions revealed that the metal nanoparticles transformed gradually from spherical-shape to larger needle-shaped crystals. Two types of Ostwald ripening processes were observed. One involves rapid aggregation of the incipient nanoparticle catalyst (2-5 nm) into blackberry-like assemblies (100-200 nm), which is accompanied with the much slower dissolution of small crystals or amorphous nanoparticles and the formation of larger needle-shaped crystals. The observed structural changes provided new insights into the durability of the polymer nanoparticle composite catalyst.

Synthesis and catalytic activity of a poly(N,N-dialkylcarbodiimide)/palladium nanoparticle composite: a case in the Suzuki coupling reaction using microwave and conventional heating.

Poly(N,N-dialkylcarbodiimide) was found to be an effective polymeric ligand system for preparing and stabilizing palladium nanoparticles (1-5 nm). The composite material prepared in situ was found to be a robust catalyst for the Suzuki coupling reaction under microwave or regular heating.

Photochemical patterning of a self-assembled monolayer of 7-diazomethylcarbonyl-2,4,9-trithiaadmantane on gold films via Wolff rearrangement.

Photolithographic attachment of functional organic molecules via ester or amide linkages to self-assembled monolayers (SAMs) on gold thin films was achieved by employing a novel photoreactive surface anchor, 7-diazomethylcarbonyl-2,4,9-trithiaadmantane. The photoreactive SAM was prepared by the spontaneous physical adsorption of the photoreactive surface anchor onto gold surfaces. The alpha-diazo ketone moiety of the SAM was found to display the classical Wolff rearrangement reactivity to produce a ketene intermediate on the exposed area. Organic molecules such as alcohols and amines can thus be attached to the gold surfaces selectively by the facile in situ formation of ester or amide linkages. The structure and reactivity of the photoreactive surface anchor were characterized by real-time FT-IR, fluorescence, and polarization modulation infrared reflectance absorption spectroscopy (PM-IRRAS). The Wolff rearrangement reactivity of the SAM suggested that a "surface-isolated" carbonylcarbene may be generated when the SAM was exposed to 255-nm irradiation.