Hydrophobic Solid Photothermal Slippery Surfaces with Rapid Self-repairing, Dual Anti-icing/Deicing, and Excellent Stability Based on Paraffin and Etching.

Ice and snow disasters have greatly affected both the global economy and human life, and the search for efficient and stable anti-icing/deicing coatings has become the main goal of much research. Currently, the development and application of anti-icing/deicing coatings are severely limited due to their complex preparation, structural fragility, and low stability. This work presents a method for preparing hydrophobic solid photothermal slippery surfaces (SPSS) that exhibit rapid self-repairing, dual anti-icing/deicing properties, and remarkable stability. A photothermal layer of copper oxide (CuO) was prepared by using chemical deposition and etching techniques. The layer was then impregnated with stearic acid and solid paraffin wax to create a hydrophobic solid photothermal slippery surface. This solves the issue of low stability on superhydrophobic surfaces caused by fragile and irretrievable micro/nanostructures. In addition, the underlying photothermal superhydrophobic surface provides good anti-icing/deicing properties even if the paraffin on the surface evaporates or is lost during operation. The findings indicate that when subjected to simulated light irradiation, the coating's surface temperature increases to 80 °C within 12 min. The self-repair process is completed rapidly in 170 s, and at -15 °C, it takes only 201 s for the ice on the surface to melt completely. The surface underneath the paraffin exhibited good superhydrophobic properties, with a contact angle (CA) of 154.1° and a sliding angle (SA) of 6.8° after the loss of paraffin. Simultaneously, the surface's mechanical stability and durability, along with its self-cleaning and antifouling properties, enhance its service life. These characteristics provide promising opportunities for practical applications that require long-term anti-icing/deicing surfaces.

The optimal intravesical maintenance chemotherapy scheme for the intermediate-risk group non-muscle-invasive bladder cancer.

OBJECTIVE: Although the current European Association of Urology(EAU) guideline recommends that patients with intermediate-risk non-muscle-invasive bladder cancer (NMIBC) should accept intravesical chemotherapy or Calmette-Guerin (BCG) for no more than one year after transurethral resection of bladder tumor(TURBT), there is no consensus on the optimal duration of chemotherapy. Hence, we explored the optimal duration of maintenance intravesical chemotherapy in patients with intermediate-risk NMIBC. SUBJECTS AND METHODS: This was a real-world single-center retrospective cohort study. In total 158 patients with pathologically confirmed intermediate-risk NMIBC were included, who were divided into 4 subgroups based on the number of instillations given. We used Cox regression analysis and survival analysis chart to explore the 3-yr recurrence outcomes of tumor.The optimal duration was determined by receive operating characteristic curve (ROC). RESULTS: The median follow-up was 5.2 years. Compared with instillation for 1-2 months, the Hazard Ratios(HR) values of instillation for less than 1 month, maintenance instillation for 3-6 months and > 6 months were 3.57、1.57 and 0.22(95% CI 1.27-12.41;0.26-9.28;0.07-0.80, P = 0.03;0.62;0.02, respectively). We found a significant improvement in 3-yr relapse-free survival in intermediate-risk NMIBC patients who maintained intravesical instillation chemotherapy for longer than 6 months, and the best benefit was achieved with 10.5 months of maintenance chemotherapy by ROC. CONCLUSIONS: In our scheme, the optimal duration of intravesical instillation with pirrubicin is 10.5 months. This new understanding provides valuable experience for the precise medical treatment model of intermediate-risk NMIBC.

Puerarin prevents sepsis-associated encephalopathy by regulating the AKT1 pathway in microglia.

BACKGROUND: Previous studies have reported that puerarin possesses cardioprotective, vasodilatory, anti-inflammatory, anti-apoptotic, and hypoglycemic properties. However, the impact of puerarin on sepsis-associated encephalopathy (SAE) remains unexplored. In this study, we explored whether puerarin can modulate microglia-mediated neuroinflammation for the treatment of SAE and delved into the underlying mechanisms. METHODS: We established a murine model of SAE through intraperitoneal injection of lipopolysaccharide (LPS). The puerarin treatment group received pretreatment with puerarin. For in vitro experiments, BV2 cells were pre-incubated with puerarin for 2 h before LPS exposure. We employed network pharmacology, the Morris Water Maze (MWM) test, Novel Object Recognition (NOR) test, immunofluorescence staining, enzyme-linked immunosorbent assay (ELISA), Western blotting, and quantitative real-time PCR (qRT-PCR) to elucidate the molecular mechanism of underlying puerarin's effects in SAE treatment. RESULTS: Our findings demonstrate that puerarin significantly reduced the production of inflammatory cytokines (TNF-α and IL-6) in the peripheral blood of LPS-treated mice. Moreover, puerarin treatment markedly ameliorated sepsis-associated cognitive impairment. Puerarin also exhibited inhibitory effects on the release of TNF-α and IL-6 from microglia, thereby preventing hippocampal neuronal cell death. Network pharmacology analysis identified AKT1 as a potential therapeutic target for puerarin in SAE treatment. Subsequently, we validated these results in both in vitro and in vitro experiments. Our study conclusively demonstrated that puerarin reduced LPS-induced phosphorylation of AKT1, with the AKT activator SC79 reversing puerarin's anti-inflammatory effects through the activation of the AKT1 signaling pathway. CONCLUSION: Puerarin exerts an anti-neuroinflammatory effect against SAE by modulating the AKT1 pathway in microglia.

Exploring hospitality workers' career choices in the wake of COVID-19: Insights from a phenomenological inquiry.

The COVID-19 pandemic severely hit the hospitality industry and caused employees concerns over health, finance, and well-being. These challenges may trigger their decisions to leave the profession, leading to major talent crises in the industry. Guided by the transactional model of stress and coping and the career construction theory, this study explored how their experiences with the pandemic affected their career choices moving on. A phenomenological approach was adopted, and 31 current and past hospitality employees were interviewed. The findings supported the conceptual model and addressed the connection between stress management and career decisions among the participants. It is also noted that, besides generational differences, most participants' career decisions at this critical moment were influenced by their personality traits, industry involvement, and employer-employee relationships. Thus, to create a sustainable, resilient, and engaged workforce, hospitality practitioners must commit to crafting positive relationships with their employees both in regular and crisis times.

Activated AMPK-mediated glucose uptake and mitochondrial dysfunction is critically involved in the glutamate-induced oxidative injury in HT22 cell.

BACKGROUND: Accumulation of glutamate damages neurons via the reactive oxygen species (ROS) injury, which was involved in the development of neurodegenerative diseases. However, the mechanism of neuronal oxidative stress damage caused by glutamate and the intervention targets still needs to be further studied. This study explored whether 5' adenosine monophosphate-activated protein kinase (AMPK)-induced glucose metabolic and mitochondrial dysfunction were related to glutamate-dependent ROS injury of the neuron. METHODS: Neuronal oxidative stress injury was induced by glutamate treatment in HT-22 cells. Western blotting was used to evaluate the phosphorylation of the AMPK. The XF24 Flux Analyzer was used to measure the effect of glutamate and Compound C (a well-known pharmacological inhibitor of AMPK phosphorylation) on the cellular oxygen consumption rate (OCR) of HT-22 cells. Glucose uptake, intracellular ROS, mitochondrial potential, apoptosis and cell viability were quantified using biochemical assays. RESULTS: Glutamate caused the phosphorylation of AMPK and subsequently promoted the glucose uptake. Furthermore, AMPK-mediated glucose uptake enhanced OCR and increased the intracellular ROS levels in neurons. The pharmacological inhibition of AMPK phosphorylation by Compound C attenuated glutamate-induced toxicity in HT22 cells by regulating the glucose uptake/mitochondrial respiration/ROS pathway. CONCLUSIONS: The AMPK phosphorylation/glucose uptake/mitochondrial respiration/ROS pathway was involved in glutamate-induced excitotoxic injury in HT22 cells. The inhibition of AMPK phosphorylation may be a potential target for the development of therapeutic agents for treating the glutamate-induced neurotoxicity.

Endothelial cell metabolism in sepsis.

BACKGROUND: Endothelial dysfunction in sepsis is a pathophysiological feature of septic organ failure. Endothelial cells (ECs) exhibit specific metabolic traits and release metabolites to adapt to the septic state in the blood to maintain vascular homeostasis. METHODS: Web of Science and PubMed were searched from inception to October 1, 2022. The search was limited to the English language only. Two reviewers independently identified studies related to EC metabolism in sepsis. The exclusion criteria were duplicate articles according to multiple search criteria. RESULTS: Sixty articles were included, and most of them were cell and animal studies. These studies reported the role of glycolysis, oxidative phosphorylation, fatty acid metabolism, and amino acid metabolism in EC homeostasis. including glycolysis, oxidative phosphorylation, fatty acid metabolism and amino acid metabolism. However, dysregulation of EC metabolism can contribute to sepsis progression. CONCLUSION: There are few clinical studies on EC metabolism in sepsis. Related research mainly focuses on basic research, but some scientific problems have also been clarified. Therefore, this review may provide an overall comprehension and novel aspects of EC metabolism in sepsis.

The Gut Microbiome and Ferroptosis in MAFLD.

Metabolic-associated fatty liver disease (MAFLD) is a new disease definition, and is proposed to replace the previous name, nonalcoholic fatty liver disease (NAFLD). Globally, MAFLD/NAFLD is the most common liver disease, with an incidence rate ranging from 6% to 35% in adult populations. The pathogenesis of MAFLD/NAFLD is closely related to insulin resistance (IR), and the genetic susceptibility to acquired metabolic stress-associated liver injury. Similarly, the gut microbiota in MAFLD/NAFLD is being revaluated by scientists, as the gut and liver influence each other via the gut-liver axis. Ferroptosis is a novel form of programmed cell death caused by iron-dependent lipid peroxidation. Emerging evidence suggests that ferroptosis has a key role in the pathological progression of MAFLD/NAFLD, and inhibition of ferroptosis may become a novel therapeutic strategy for the treatment of NAFLD. This review focuses on the main mechanisms behind the promotion of MAFLD/NAFLD occurrence and development by the intestinal microbiota and ferroptosis. It outlines new strategies to target the intestinal microbiota and ferroptosis to facilitate future MAFLD/NAFLD therapies.

A Slippery Liquid-Infused Network-like Surface with Anti/De-icing Properties Constructed Based on the Phosphating Reaction.

The excessive accumulation of ice seriously threatens various industrial facilities and production activities. Currently, slippery liquid-injected porous surfaces (SLIPS) have been developed as a new strategy for anti/de-icing; however, the lack of research on the adsorption and storage capacity for lubricating fluids has limited the development of SLIPS in the anti/de-icing field to some extent. In this work, a slippery liquid-infused phosphate network-like surface (SLIPNS) is prepared that adjusts the texture of the surface by varying the phosphating time to control the adsorption and storage of lubricating fluids. The as-obtained surface structure gives the SLIPNS excellent oil-storage/locked properties, can delay the freezing time of sessile droplets up to 436 s, which is almost 10 times that of an untreated aluminum sheet, and exhibits one-tenth the ice adhesion strength of untreated aluminum substrates (14.39 kPa). In addition, the SLIPNS shows effective durability and antifouling ability and has great potential in solving long-term anti/de-icing problems.

COVID-19 prevention in hotels: Ritualized host-guest interactions.

As COVID-19 prevention efforts have become normalized, conflicts between guests and hotel staff, who must adhere to government protocols, can have a serious impact on host-guest interactions. Drawing on interaction ritual chain theory, this research explores the ritualized mechanism of host-guest interactions during the pandemic from the perspectives of staff and guests. By combining video ethnography and interviews, this study identifies the ritual ingredients, processes, outcomes, and collective symbols of COVID-19 prevention measures. Based on the attitudes and performance paths of staff and guests, the interaction chain may become longer or shorter, and result in guests becoming "insiders" or "outsiders" and leaving the interaction space. An integrated model of host-guest interactions based on interaction ritual theory is proposed.

Laparoscopic versus open reduction of idiopathic intussusception in children: an updated institutional experience.

BACKGROUND: In the reduction of intussusception, due to the lack of randomized, controlled, and prospective clinical trials to confirm the superiority of the laparoscopic approach over open surgery, more evidence was needed. This study aimed to compare the results of laparoscopy and open reduction of idiopathic intussusception in children as well as to illustrate some skills for the reduction of intussusception laparoscopically. METHODS: A retrospective review was performed to evaluate outcomes for patients with idiopathic intussusception who were treated laparoscopically (LAP group) from January 2015 to December 2019 and to compare the outcomes with laparotomy (OPEN group) during the same period. RESULTS: During the period studied, there were 162 patients treated surgically for intussusception: 62 LAP and 100 OPEN. No statistical differences were found in demographic data, clinical symptoms and signs, duration of symptoms, location and types of intussusception between the two groups. Conversion to open procedure was required for 11 patients in the LAP group. The operation time and time to oral intake were shorter in the LAP group while the difference was not significant. If the 11 conversion cases were excluded, the operation time and time to oral intake were significantly shorter (P < 0.05) in the LAP group. The length of stay was significantly shorter in the LAP group (P < 0.05). Intraoperative and postoperative complication rates between the two groups were comparable (P = 1.0). CONCLUSION: Laparoscopy was safe and effective in the treatment of pediatric idiopathic intussusceptions. Pediatric surgeons with sophisticated minimally invasive skills should choose laparoscopy as the first choice in the treatment of idiopathic intussusceptions.

Multicolor fluorescence switching material induced by force and acid.

A novel D-A-D chromophore TBQM based on triphenylamine, acylhydrazone and dimethylamino was synthesized, and the emission properties of TBQM was studied in solutions as well as in aggregated state. TBQM showed obvious solvatochromism in different solutions. In addition, the reversible multicolor fluorescence switching properties under the stimulation of external forces and acid were also obtained. The fluorescence of TBQM changed from blue to bright blue, and finally to blue-green as the degree of grinding increased, which would recover after being fumigated by CH2Cl2. Meanwhile, TBQM could undergo twice protonation after fumigated by TFA. The fluorescence color changed from blue to bright blue, blue-green, and yellow-green until the fluorescence was quenched with the increasing of TFA fumigation time, which can be restored automatically or by TEA fumigation. Moreover, TBQM could be used as an advanced fluorescent anti-counterfeiting ink.

MutT Homolog 1 Inhibitor Karonudib Attenuates Autoimmune Hepatitis by Inhibiting DNA Repair in Activated T Cells.

Autoimmune hepatitis (AIH) is an inflammatory liver disease driven by the hyperactivation of various intrahepatic antigen-specific T cells due to a breach of immune tolerance. Studies in immunometabolism demonstrate that activated T cells harbor increased levels of reactive oxygen species that cause oxidative DNA damage. In this study, we assessed the potential of DNA damage repair enzyme MutT homolog 1 (MTH1) as a therapeutic target in AIH and karonudib as a novel drug for patients with AIH. We report herein that MTH1 expression was significantly increased in liver samples from patients with AIH compared to patients with chronic hepatitis B and nonalcoholic fatty liver disease and from healthy controls. In addition, the expression of MTH1 was positively correlated with AIH disease severity. We further found abundant T cells that expressed MTH1 in AIH. Next, we found that karonudib significantly altered T-cell receptor signaling in human T cells and robustly inhibited proliferation of human T cells in vitro. Interestingly, our data reflected a preferential inhibition of DNA damage repair in activated T cells by karonudib. Moreover, MTH1 was required to develop liver inflammation and damage because specific deletion of MTH1 in T cells ameliorated liver injury in the concanavalin A (Con A)-induced hepatitis model by inhibiting T-cell activation and proliferation. Lastly, we validated the protective effect of karonudib on the Con A-induced hepatitis model. Conclusion: MTH1 functions as a critical regulator in the development of AIH, and its inhibition in activated T cells reduces liver inflammation and damage.

Force-, heat- and acid-induced fluorescent switching properties of an anthracene-based hydrazide derivative.

A novel anthracene-based hydrazide derivative (3,4-ENS) was designed and synthesized, and 3,4-ENS can form stable organogel in dimethyl sulfoxide (DMSO) solvent. Firstly, 3,4-ENS xerogel from DMSO exhibits mechanofluorochromic property and its maximum emission shifts from 433 nm to 484 nm upon grinding. Secondly, DMSO xerogel exhibits thermofluorochromic behavior and its maximum emission shifts from 433 nm to 481 nm upon heating at 110 °C. Thirdly, DMSO xerogel exhibits acidofluorochromic behavior and its maximum emission shifts from 433 nm to 466 nm upon fuming by TFA vapors. The experimental results confirmed that the different luminescent property of 3,4-ENS attributed to the phase transition from well-ordered crystals to metastable disordered aggregation.

Artemisinin improves neurocognitive deficits associated with sepsis by activating the AMPK axis in microglia.

Sepsis is life-threatening organ dysfunction due to dysregulated systemic inflammatory and immune response to infection, often leading to cognitive impairments. Growing evidence shows that artemisinin, an antimalarial drug, possesses potent anti-inflammatory and immunoregulatory activities. In this study we investigated whether artemisinin exerted protective effect against neurocognitive deficits associated with sepsis and explored the underlying mechanisms. Mice were injected with LPS (750 µg · kg-1 · d-1, ip, for 7 days) to establish an animal model of sepsis. Artemisinin (30 mg · kg-1 · d-1, ip) was administered starting 4 days prior LPS injection and lasting to the end of LPS injection. We showed that artemisinin administration significantly improved LPS-induced cognitive impairments assessed in Morris water maze and Y maze tests, attenuated neuronal damage and microglial activation in the hippocampus. In BV2 microglial cells treated with LPS (100 ng/mL), pre-application of artemisinin (40 µΜ) significantly reduced the production of proinflammatory cytokines (i.e., TNF-α, IL-6) and suppressed microglial migration. Furthermore, we revealed that artemisinin significantly suppressed the nuclear translocation of NF-κB and the expression of proinflammatory cytokines by activating the AMPKα1 pathway; knockdown of AMPKα1 markedly abolished the anti-inflammatory effects of artemisinin in BV2 microglial cells. In conclusion, atemisinin is a potential therapeutic agent for sepsis-associated neuroinflammation and cognitive impairment, and its effect is probably mediated by activation of the AMPKα1 signaling pathway in microglia.

An Hypothesis: Disproportion Between Cardiac Troponin and B-Type Natriuretic Peptide Levels-A High Risk and Poor Prognostic Biomarker in Patients With Fulminant Myocarditis?

In our clinical practice, we recently found some patients with severe fulminant myocarditis (FM) who showed persistently elevated cardiac troponin (cTn) levels and "seemingly normal" B-type natriuretic peptide (BNP) level, and who subsequently progressed to poor outcomes. Indeed, this sounds contrary to conventional wisdom, but it is not an accidental phenomenon. Fulminant myocarditis is a rapidly progressive disease associated with high mortality. Recent studies have shown that patients with FM are significantly more likely to require heart transplantation than those without FM. Prompt diagnosis of FM and the institution of advanced cardiac life support will save more lives. Cardiac troponin and BNP are widely used diagnostic markers. Cardiac troponin is a specific marker of cardiac injury and its level correlates with the severity of cardiac injury. However, plasma BNP has a dual identity; it is not only a marker of cardiac pressure/volume overload, but it is also a cardioprotective factor that provides effective neurohormonal compensation to maintain homeostasis. Similar to fulminant hepatitis (characterised by diffuse inflammation and massive parenchymal cell necrosis) sometimes showing disproportion between transaminase level and bilirubin level, the disproportion between cTn and BNP levels in FM seems to be consistent with its severe histopathological changes, including diffuse infiltration of the myocardium by inflammatory cells, as well as severe cardiomyocyte injury and necrosis. Moreover, in previous studies, a lower BNP level was found to be an adverse prognostic marker in end-stage heart failure. All these findings indicate that in patients with FM with a persistently high cTn level and ominous clinical presentation, a "seemingly normal" BNP level is not a friendly signal. We hypothesise that the combination of a persistently elevated cTn level and low BNP level in patients with FM indicates worse myocardial injury and poor prognosis.

FOXD1-AS1 regulates FOXD1 translation and promotes gastric cancer progression and chemoresistance by activating the PI3K/AKT/mTOR pathway.

Gastric cancer (GC) is a common gastrointestinal cancer with a high global mortality. Recent reports have suggested that long noncoding RNA (lncRNA) are implicated in multiple aspects of GC, including pathogenesis, progression, and therapeutic response. Herein, we investigated the function of FOXD1-AS1 in GC progression and chemoresistance. Expression of FOXD1-AS1 was low in normal stomach tissues but was upregulated in GC cell lines. Silencing of FOXD1-AS1 impaired GC cell proliferation and motility in vitro, and repressed tumor growth and metastasis in vivo. Importantly, FOXD1-AS1 upregulation increased the resistance of GC cells to cisplatin. Moreover, we found that FOXD1-AS1 promoted FOXD1 protein translation through the eIF4G-eIF4E-eIF4A translational complex. We also demonstrated that FOXD1-AS1 released eIF4E from phosphorylated 4E-BP1 and thereby strengthened the interaction of eIF4E with eIF4G by activating the PI3K/AKT/mTOR pathway. Activation of the PI3K/AKT/mTOR pathway was due to the post-transcriptional upregulation of PIK3CA, in turn induced by FOXD1-AS1-mediated sequestering of microRNA (miR)-466. Furthermore, we verified that FOXD1-AS1 facilitated GC progression and cisplatin resistance in a FOXD1-dependent manner. In conclusion, FOXD1-AS1 aggravates GC progression and chemoresistance by promoting FOXD1 translation via PIK3CA/PI3K/AKT/mTOR signaling. These findings highlight a novel target for treatment of patients GC, particularly patients with cisplatin resistance.

lncRNA SNHG11 Promotes Gastric Cancer Progression by Activating the Wnt/ß-Catenin Pathway and Oncogenic Autophagy.

Long non-coding RNAs (lncRNAs) are under active investigation in the development of cancers, including gastric cancer (GC). Oncogenic autophagy is required for cancer cell survival. The present study aimed to investigate the regulatory role of lncRNA small nucleolar host gene 11 (SNHG11) in GC. We show that SNHG11 is upregulated in GC, and that its upregulation correlated with dismal patient outcomes. Functionally, SNHG11 aggravated oncogenic autophagy to facilitate cell proliferation, stemness, migration, invasion, and epithelial-to-mesenchymal transition (EMT) in GC. Mechanistically, SNHG11 post-transcriptionally upregulated catenin beta 1 (CTNNB1) and autophagy related 12 (ATG12) through miR-483-3p/miR-1276, while the processing of precursor (pre-)miR-483/pre-miR-1276 was hindered by SNHG11. SNHG11 induced GSK-3ß ubiquitination through interacting with Cullin 4A (CUL4A) to further activate the Wnt/ß-catenin pathway. Intriguingly, SNHG11 regulated autophagy in a manner dependent on ATG12 rather than the Wnt/ß-catenin pathway, whereas SNHG11 contributed to the malignant behaviors of GC cells via both pathways. Finally, SNHG11 upregulation in GC cells was shown to be transcriptionally induced by TCF7L2. In conclusion, we reveal that SNHG11 is an onco-lncRNA in GC and might be a promising prognostic and therapeutic target for GC.

APCCDC20-mediated degradation of PHD3 stabilizes HIF-1a and promotes tumorigenesis in hepatocellular carcinoma.

CDC20 regulates cell cycle progression by targeting key substrates for destruction, but its role in hepatocellular carcinoma (HCC) tumorigenesis remains to be explored. Here, by using weighted gene co-expression network analysis (WGCNA), we identified CDC20 as a hub gene in HCC. We demonstrated that CDC20 expression is correlated with HIF-1 activity and overall survival (OS) of clinic HCC patients. The activity of HIF-1 is regulated by the stability of HIF-1a subunit, which is hydroxylated by oxygen-dependent prolyl hydroxylase enzymes, the PHDs. In addition, we show that genetic ablation or pharmacological inhibition of CDC20 can accelerate the degradation of HIF-1a and impair VEGF secretion in HCC cells. Mechanistically, we found that CDC20 binds to the destruction-box (D-box) motif present in the PHD3 protein to promote its polyubiquitination and degradation. The depletion of endogenous PHD3 in CDC20 knockdown HCC cells greatly attenuated the decline of HIF-1a protein and restored the secretion of VEGF. In contrast, overexpression of a non-degradable PHD3 mutant significantly inhibited the proliferation of HCC cells both in vitro and in vivo. Collectively, our findings indicate that CDC20 plays a crucial role in the development of HCC by governing PHD3 protein.

Targeting LncRNA EPIC1 to inhibit human colon cancer cell progression.

Long non-coding RNA EPIC1 (Lnc-EPIC1) binds MYC protein, which is essential for MYC function and expression of MYC target genes. The current study tested its expression and potential functions in human colon cancer cells. We show that Lnc-EPIC1 expression is elevated in human colon cancer tissues and primary human colon cancer cells. Whereas its expression is relatively low in normal colon tissues and colon epithelial cells. In the primary human colon cancer cells, Lnc-EPIC1 siRNA largely inhibited cancer cell growth, proliferation, migration and invasion. Further, Lnc-EPIC1 silencing induced significant apoptosis activation in colon cancer cells. Conversely, ectopic overexpression of Lnc-EPIC1 augmented colon cancer cell growth, proliferation, migration and invasion. RNA-immunoprecipitation and RNA pull-down results confirmed that Lnc-EPIC1 directly binds MYC protein in colon cancer cells. MYC target proteins, including cyclin A, cyclin D and CDK9, were downregulated with Lnc-EPIC1 silencing, but upregulated after Lnc-EPIC1 overexpression in colon cancer cells. Further Lnc-EPIC1 silencing or overexpression failed to alter functions of MYC-knockout colon cancer cells. Collectively, overexpressed Lnc-EPIC1 is important for the progression of human colon cancer cells.

Stimuli-responsive behavior of naphthyl acylhydrazone derivative and its application in information security protection.

Acylhydrazone derivatives containing naphthyl group, namely, 3,5-bis-octyloxy-benzoic acid naphthalen-1-ylmethylene-hydrazide (NTH-mB8) and 4-methoxy-benzoic acid naphthalen-1-ylmethylene-hydrazide (NTH-P1) were synthesized. π-π interactions between naphthalene groups and -N-H···O=C- intermolecular hydrogen bondings were observed in NTH-P1 single crystal, in which -C=N- bonds exhibited trans-isomer. NTH-mB8 showed photo-responsive behavior due to photo-induced trans-cis isomerizations of -C=N- bonds. Interestingly, the NTH-mB8 films fumed by trifluoroacetic acid (TFA)/triethylamine (TEA) (or standing at room temperature) vapors show reversible fluorescence on/off switching property. The cast film of NTH-mB8 exhibited almost no fluorescence. The NTH-mB8 film fumed by TFA vapor exhibited intensive cyan emission, which was quickly quenched by TEA vapor. The reversible remarkable fluorescence on/off switching properties suggested that the organic solution of NTH-mB8 could be used as security ink without needing a covering reagent in information security protection.