Norfloxacin versus alternative antibiotics for prophylaxis of spontaneous bacteria peritonitis in cirrhosis: a systematic review and meta-analysis.

BACKGROUND: Spontaneous bacterial peritonitis (SBP) is a life-threatening complication in patients with advanced cirrhosis. Prophylactic Norfloxacin used to be considered effective in SBP prevention, but in recent years its efficacy has been partially compromised by increasing quinolone-resistant bacteria. However, whether the effects of alternative prophylactic regimens are superior to norfloxacin remains controversial. The goal of this study is to compare the effects of norfloxacin with other antibiotics in SBP prophylaxis for cirrhotic patients. METHODS: We systematically searched Pubmed, Embase, and Cochrane Library Databases. Two reviewers independently identified relevant random control trials (RCTs) comparing the role of norfloxacin and other antibiotics in SBP prevention. RESULTS: Eight studies comprising 1043 cirrhotic patients were included in this study. Norfloxacin and alternative antibiotics displayed comparable effects in SBP prophylaxis, survival benefit, overall infection prevention, and safety. Subgroup analyses revealed that rifaximin prophylaxis could reduce the recurrence of SBP with fewer adverse events but failed to improve overall survival compared with norfloxacin. CONCLUSIONS: Other antibiotics are a reasonable alternative to norfloxacin in the prophylaxis of SBP. Rifaximin prophylaxis could be an alternative choose of antibiotic for SBP prevention because of its better protective effect and safety.

Downregulation of SLC9A8 Promotes Epithelial-Mesenchymal Transition and Metastasis in Colorectal Cancer Cells via the IL6-JAK1/STAT3 Signaling Pathway.

BACKGROUND: SLC9A8 has been shown to be involved in mucus layer formation, intestinal mucosal integrity, and hyperproliferation of colitis-associated tumor development. However, its effects on the epithelial-mesenchymal transition (EMT) and the metastasis of colorectal cancer (CRC) remain unknown. AIMS: To explore whether SLC9A8 participates in EMT and the metastasis of CRC. METHODS: Western blotting and immunohistochemistry were performed to evaluate the expression of SLC9A8 in CRC patients. At the cellular level, the effect of SLC9A8 on proliferation, migration, and invasion was measured using cell viability analysis, flow cytometry analysis, and Transwell assays. Mouse tumor xenograft and metastasis models were established to analyze whether knockdown of SLC9A8 increased tumor volume, tumor weight, and metastasis. Moreover, whether downregulated expression of SLC9A8 promotes EMT via activation of the IL6-JAK1-STAT3 signaling pathway was investigated. RESULTS: SLC9A8 protein was downregulated in CRC tissues, and this downregulation was significantly associated with tumor size, lymph node status, pTNM stage, and poor prognosis. SLC9A8 overexpression markedly suppressed cell proliferation, migration, and invasion. Downregulation of SLC9A8 promoted CRC cell proliferation, migration, and invasion. Moreover, knockdown of SLC9A8 also increased tumor volume, tumor weight, and metastasis in vivo. Meanwhile, downregulation of SLC9A8 significantly promoted the in vitro migration of CRC cells via EMT by activating the IL6-JAK1/STAT3 signaling pathway. CONCLUSIONS: Downregulation of SLC9A8 plays an important role in EMT and metastasis of CRC progression and may become a new potential therapeutic target for the treatment of CRC.

CTCF-silenced miR-137 contributes to EMT and radioresistance in esophageal squamous cell carcinoma.

BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is one of the most malignant tumors in gastrointestinal system. MicroRNAs (miRNAs) have been reported to be implicated in cancer development. However, the role of miR-137 has not been fully revealed in ESCC. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot analyses were separately used to examine RNA level and protein level. 5-ethynyl-2'-deoxyuridine (EdU) assay, transwell assays and flow cytometry analyses were conducted to assess biological behaviors of ESCC cells. Additionally, the interaction between genes were analyzed via Chromatin Immunoprecipitation (ChIP) assay, RNA Binding Protein Immunoprecipitation (RIP) assay, RNA pull down assay and luciferase reporter assay. RESULTS: MiR-137 was down-regulated in ESCC cells. Upregulation of miR-137 hindered ESCC cell proliferation, migration, invasion and epithelial mesenchymal transition (EMT). Besides, miR-137 enhanced the sensitivity of ESCC cells to irradiation. Moreover, CCCTC-binding factor (CTCF) inactivated miR-137 transcription in ESCC cells. Furthermore, we revealed enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) and paxillin (PXN) as the downstream targets of miR-137. In turn, EZH2 was recruited by CTCF and induced methylation in miR-137 promoter. CONCLUSION: CTCF/Suz12/EZH2 complex-silenced miR-137 facilitates ESCC progression and radioresistance by targeting EZH2 and PXN.

Excessive Body Fat at a Young Age Increases the Risk of Colorectal Cancer: A Systematic Review and Meta-Analysis.

Overweight and obesity was considered as a risk factor for colorectal cancer (CRC), and CRC development may be due to exposure during one's youth. Metabolic syndrome and insulin resistance seem to play an important role in the underlying mechanisms. Even though several studies indicated the association between BMI at young age and CRC risks, an identified founding is still lacked. Therefore, we conducted a meta-analysis and a dose-response analysis to quantify the association between BMI at young age and CRC risks with relative accuracy. We searched the PubMed, Embase, Medline and Cochrane Library databases for articles published before Sep. 15, 2019. Fifteen articles with 2 520 091 participants were included. Risk for CRC was estimated using relative risks (RR) and 95% confidence intervals (CIs). Compared with individuals with normal weight, overweight and obese young adults had a significantly higher risk of CRC (relative risks (RR):18%, 95% CI:1.08, 1.28； RR:32%, 95% CI: 1.11, 1.56, respectively). However, this correlation may not exist for obese women (RR: 1.22, 95% CI: 0.99, 1.51); Overweight may not a risk factor for rectal cancer (RC) (RR: 1.12, 95% CI: 0.97, 1.29). In the dose-response analysis, we observed a linear relationship between BMI at a young age and CRC risk, with each 1 kg/m2 increment associated with a 2% increased risk. Higher BMI at a young age was positively associated with CRC risk, which indicates that weight control since a young age was needed.

Comparable safety of ERCP in symptomatic and asymptomatic patients with common bile duct stones: a propensity-matched analysis.

BACKGROUND: The safety of endoscopic retrograde cholangiopancreatography (ERCP) for asymptomatic common bile duct (CBD) stones patients has not been thoroughly elucidated. This study attempted to compare the incidence and severity of ERCP complications in asymptomatic and symptomatic patients with CBD stones and to provide evidence for the treatment of asymptomatic CBD stones. METHODS: The clinical data of patients were retrospectively analyzed. These patients were divided into the asymptomatic CBD stones group and the symptomatic CBD stones group. Propensity score matching (PSM) was used to match the two groups. The incidence and severity of postoperative complications of ERCP in the two groups were analyzed. RESULTS: A total of 79 patients who had asymptomatic CBD stones and 795 patients who had symptomatic CBD stones were included in this study. After PSM, 79 patients from the asymptomatic CBD group and 316 patients from the symptomatic CBD stones group were identified. Before and after PSM, no significant differences in the incidence and severity of post-ERCP pancreatitis (PEP) were noted between the two groups (p > .05). In addition, no differences in the incidence and severity of other complications, including acute cholangitis, bleeding and perforation, between the two groups were observed before and after PSM (p > .05). CONCLUSIONS: Patients with asymptomatic CBD stones do not exhibit an increased risk of ERCP-related complications compared with those with symptomatic CBD stones. ERCP was observed to be equally safe and efficacious for patients with asymptomatic versus symptomatic CBD stones.

Trioctylphosphine accelerated growth of InP quantum dots at low temperature.

Significant advance was realized on the economic synthesis of InP quantum dots (QDs) by using aminophosphines as phosphorus precursor. However, the low reaction activity and thermal degradation of aminophosphines bring severe difficulty for growth control of InP QDs. Here, we employed trioctylphosphine (TOP) as a surfactant to accelerate the growth of the InP QDs. The reaction mechanism study reveals that the TOP could form a reactive complex with indium halides that effectively accelerates the formation of InP monomer and reduces the demand for reaction temperature. On this basis, the effect of reaction temperature, precursors, and zinc halide additives on the growth of the TOP-InP QDs was explored. This strategy alleviates the difficulty in growth control of InP QDs and also benefits to the synthesis of luminescent InP/ZnS core-shell QDs within visible regime. A white-light emitting diode device was fabricated with the InP/ZnS QDs that demonstrates their application potential in light-emitting devices.

Somatostatin stimulates colonic MUC2 expression through SSTR5-Notch-Hes1 signaling pathway.

Colonic mucus barrier is regarded as the first defense line against bacteria and antigens from directly attaching to the epithelium, which would further lead to intestinal inflammation activation and pathological conditions. As MUC2 mucin is the predominant component of the mucus, understanding the regulatory mechanisms of MUC2 is important for mucus barrier protection. Somatostatin (SST) has been found to play a role in colon protection through various manners. However, whether SST involves in colonic mucus barrier regulation is still unclear. The aim of this study is to investigate the effects and potential mechanisms of SST on colonic MUC2 expression and mucus secretion. In vivo study, exogenous somatostatin (octreotide) administration effectively stimulated mice colonic MUC2 expression and mucus secretion. In human goblet-like cell LS174T cells, SST exposure also significantly stimulated MUC2 expression and mucus secretion. Further studies indicated that SST receptor 5 (SSTR5) was significantly activated by SST, whereas specific SSTR5 siRNA transfection of LS174T cells significantly blocked SST-induced increase in MUC2 expression and mucus secretion. In addition, SSTR5 agonist L817,818 also upregulated MUC2 expression and mucus secretion in LS174T cells. Mechanistic studies further demonstrated that SST/SSTR5-mediated MUC2 upregulation was dependent on Notch-Hes1 pathway suppression by detecting notch intracellular domain (NICD) and Hes1 proteins. Taken together, our findings suggested that SST could participate in colonic mucus barrier regulation through SSTR5-Notch-Hes1-MUC2 signaling pathway. These findings provide a deep insight into the role of SST on colonic mucus regulation under physiological conditions.

Nonsteroidal anti-inflammatory drugs alleviate severity of post-endoscopic retrograde cholangiopancreatography pancreatitis by inhibiting inflammation and reducing apoptosis.

BACKGROUND AND AIM: The prophylactic effect of nonselective nonsteroidal anti-inflammatory drugs on post-ERCP (endoscopic retrograde cholangiopancreatography) pancreatitis has been observed for a long time. However, whether the selective nonsteroidal anti-inflammatory drugs possess similar abilities and the mechanisms by which nonsteroidal anti-inflammatory drugs work remain unclear. The present study aimed to determine the protective effects of nonsteroidal anti-inflammatory drugs on post-ERCP pancreatitis in a rat model and examine underlying mechanisms. METHODS: Thirty-two female rats were equally and randomly divided into four groups: the sham group, post-ERCP pancreatitis model group, indomethacin-pretreated group, and parecoxib-pretreated group. Indomethacin or parecoxib was delivered 30 min prior to surgery; 24 h after post-ERCP pancreatitis establishment, the rats were sacrificed. Serum amylase and lipase activities, inflammatory cytokine release, pancreatic histopathological scores, neutrophil infiltration, and the expression pattern cyclooxygenase at the protein level and pancreatic apoptosis were quantified and analyzed. RESULTS: Both indomethacin and parecoxib inhibited the activities of serum amylase and lipase and reduced the severity of pancreatic histopathology. Mechanistically, both drugs decreased the expression level of cyclooxygenase 2; however, they had no influence on the cyclooxygenase 1 protein level. Moreover, they reduced inflammatory cytokine release, neutrophil infiltration into the pancreas, and NF-κB p65 activation. Notably, we found that apoptotic cells in the pancreas were remarkably diminished after the administration of both nonsteroidal anti-inflammatory drugs. CONCLUSIONS: Both selective and nonselective nonsteroidal anti-inflammatory drugs exert protective effects against post-ERCP pancreatitis by restraining inflammation and reducing acinar cell apoptosis through the inhibition of cyclooxygenase 2.

A Scalable Smartwatch-Based Medication Intake Detection System Using Distributed Machine Learning.

Poor Medication adherence causes significant economic impact resulting in hospital readmission, hospital visits and other healthcare costs. The authors developed a smartwatch application and a cloud based data pipeline for developing a user-friendly medication intake monitoring system that can contribute to improving medication adherence. The developed Android smartwatch application collects activity sensor data using accelerometer and gyroscope. The cloud-based data pipeline includes distributed data storage, distributed database management system and distributed computing frameworks in order to build a machine learning model which identifies activity types using sensor data. With the proposed sensor data extraction, preprocessing and machine learning algorithms, this study successfully achieved a high F1 score of 0.977 with 13.313 seconds of training time and 0.139 seconds for testing.

White light-emitting diodes based on carbon dots and Mn-doped CsPbMnCl3 nanocrystals.

CsPbX3 perovskite nanocrystals (NCs) are becoming a promising material for optoelectronic devices that possess an optically tunable bandgap, and bright photoluminescence. However, the toxic Pb is not environmentally friendly and the quantum yield (QY) of blue emitting NCs is relatively low. In addition, the red emitting perovskite containing iodine is not stable under light illumination. In this paper, high QY, blue emitting, non-toxic fluorescent nanomaterial carbon dots and orange-emitting CsPb0.81Mn0.19Cl3 NCs with partial Pb replacement are combined to fabricate white light-emitting diodes (WLEDs). A WLED with color coordinates of (0.337, 0.324) and a correlated color temperature of 4804 K is fabricated. Compared to red emitting perovskite containing iodine, the CsPb0.81Mn0.19Cl3 NCs are stable no matter whether they are stored in the air or exposed under ultraviolet light. Therefore, the as-fabricated WLED shows good color stability against increasing currents and long-term working stability.

Controlled Growth of CH3 NH3 PbBr3 Perovskite Nanocrystals via a Water-Oil Interfacial Synthesis Method.

Fundamental insights into the reaction kinetics of organic-inorganic lead halide perovskite nanocrystals (LHP NCs) are still limited due to their ultrafast formation rate. Herein, we develop a water-oil interfacial synthesis of MAPbBr3 NCs (MA=CH3 NH3 + ), which prolongs the reaction time to tens of minutes. This method makes it possible to monitor in situ the formation process of MAPbBr3 NCs and observe successive spectral evolutions from 438 to 534 nm in a single reaction by extending reaction time. The implementation of this method depends on reducing the formation rate of PbBr6 4- octahedra and the diffusion rate of MA. The formation of PbBr6 4- is a rate-determining step, and the biphasic system offers a favorable reaction condition to control the mass transfer of MA. The effects of temperature and concentration of precursor and ligand are investigated in detail.

Molecular mechanisms of somatostatin-mediated intestinal epithelial barrier function restoration by upregulating claudin-4 in mice with DSS-induced colitis.

Intestinal barrier dysfunction plays a crucial role in the pathogenesis of ulcerative colitis (UC). Previous studies have shown somatostatin (SST) can protect intestinal barrier structure possibly through upregulating tight junction (TJ) protein expression, but the mechanisms of this upregulation remain undefined. This study aimed to investigate the molecular mechanisms of interaction of SST with its downstream regulatory elements in DSS-induced colitis mice. In DSS-induced colitis mice, exogenous SST supplement (octreotide) effectively ameliorated disease progression, restored colonic barrier structure and function, and stimulated claudin-4 expression. Similar effects were also observed for SST on Caco-2 cells intervened by TNF-α. SST receptor 5 (SSTR5) agonist L-817,818 upregulated the claudin-4 expression whereas the SSTR2 agonist seglitide could not reverse TNF-α-induced reduction of claudin-4. SST treatment significantly decreased the phosphorylation levels of ERK1/2 and p38 induced by TNF-α. PD-98059 (ERK1/2 pathway inhibitor) but not SB-202190 (p38 pathway inhibitor) could reverse TNF-α-induced suppression of claudin-4 expression. Both inhibitors could improve the TJ barrier function damaged by TNF-α. Our studies suggest that the protective effect of SST on intestinal barrier achieved by upregulating claudin-4 expression through activation of SSTR5 and suppression of the ERK1/2 pathways. These findings will benefit the development of novel treatment regimens for UC.

KIAA0101 inhibition suppresses cell proliferation and cell cycle progression by promoting the interaction between p53 and Sp1 in breast cancer.

KIAA0101 functions as a regulator of centrosome number in breast cancer. Here, we identify the role of KIAA0101 in breast cancer cell proliferation and cell cycle progression. KIAA0101 knockdown significantly inhibited cell growth, colony formation and G1/S phase transition. Further investigation indicated that KIAA0101 silencing suppressed the expression of CCNE2, CDK6 and CDKN1A. Luciferase reporter assay and ChIP assay demonstrated that Sp1 positively regulated the transcription of CCNE2, CDK6 and CDKN1A. KIAA0101 knockdown promoted the interaction between p53 and Sp1, inhibiting the transcriptional activation of Sp1 on CCNE2, CDK6 and CDKN1A. Knockdown of p53 counteracted the inhibitory effect of KIAA0101 knockdown on breast cancer cells proliferation and cell cycle progression while Sp1 knockdown mimicked the effect of KIAA0101 knockdown. These results suggested that KIAA0101 knockdown suppressed the cell proliferation and cell cycle progression by promoting the formation of p53/Sp1 complex in breast cancer.

MicroRNA-98 regulates hepatic cholesterol metabolism via targeting sterol regulatory element-binding protein 2.

Hypercholesterolemia is an important risk factor for coronary heart disease. Although a lot of research has been conducted, the regulation of cholesterol metabolism is still largely unknown. Some miRNAs have been found to play critical role in the cholesterol metabolism. MiR-98 is a miRNA whose function has been reported mainly in tumorigenesis. In this study, we elucidate a novel role of miR-98 in cholesterol metabolism. We found that the expression of miR-98 was decreased significantly in hypercholesterolemic patients compared with healthy control subjects. Furthermore, we identified that SREBP-2, an important transcriptional factor in cholesterol metabolism, was a direct target of miR-98. Overexpression of miR-98 significantly repressed the 3'-UTR reporter activities of SREBP-2 in a dose-dependent manner in HepG2 cells, while the effect of miR-98 was blocked when the binding site of miR-98 within the SREBP-2 3'-UTR was mutated. And overexpression of miR-98 reduced both the mRNA and protein levels of HMGCR and LDLR significantly in vitro, which are two target genes of SREBP-2. Furthermore, MiR-98 overexpression reduced the intracellular total cholesterol levels dramatically. Moreover, we overexpressed the miR-98 by lentiviral tail vein injection in vivo. Compared with the control mice, the miR-98 overexpression mice showed lower serum cholesterol level and decreased SREBP-2, HMGCR as well as LDLR expression. Our data confirmed that reduced expression of miR-98 potentially contributes to disturbance of cholesterol metabolism. MiR-98 might be a novel therapeutic target to hypercholesterolemia.

Up-regulation of NHE8 by somatostatin ameliorates the diarrhea symptom in infectious colitis mice model.

Na+/H+ exchangers (NHEs) have been shown to be involved in regulating cell volume and maintaining fluid and electrolyte homeostasis. Pooled evidences have suggested that loss of Na+/H+ exchanger isoform 8 (NHE8) impairs intestinal mucosa. Whether NHE8 participates in the pathology of infectious colitis is still unknown. Our previous study demonstrated that somatostatin (SST) could stimulate the expression of intestinal NHE8 so as to facilitate Na+ absorption under normal condition. This study further explored whether NHE8 participates in the pathological processes of infectious colitis and the effects of SST on intestinal NHE8 expression in the setting of infectious colitis. Our data showed that NHE8 expression was reduced in Citrobacter rodentium (CR) infected mice. Up-regulation of NHE8 improved diarrhea symptom and mucosal damage induced by CR. In vitro, a similar observation was also seen in Enteropathogenic E. coli (EPEC) infected Caco-2 cells. Seglitide, a SST receptor (SSTR) 2 agonist, partly reversed the inhibiting action of EPEC on NHE8 expression, but SSTR5 agonist (L-817,818) had no effect on the expression of NHE8. Moreover, SST blocked the phosphorylation of p38 in EPEC-infected Caco-2 cells. Taken together, these results suggest that enhancement of intestinal NHE8 expression by SST could ameliorate the symptoms of mice with infectious colitis.

Aqueous Synthesis of Methylammonium Lead Halide Perovskite Nanocrystals.

Methylammonium lead halide perovskite nanocrystals offer attractive optoelectronic properties but suffer from fast degradation in the presence of water. In contradiction to this observation, we demonstrate the possibility of a direct aqueous synthesis of CH3 NH3 PbX3 (X=Br or Cl/Br) nanocrystals through the reaction between the lead halide complex and methylamine when the pH is maintained in the range of 0-5. Under these synthetic conditions, the positively charged surface of the perovskite nanocrystals and the proper ionic balance help to prevent their decomposition in water. Additional surface capping with organic amine ligands further improves the photoluminescence quantum yield of the perovskite nanocrystals to values close to 40 %, ensures their stability under ambient conditions for several months, and their photoluminescence performance under continuous 0.1 W mm-2 405 nm light irradiation for over 250 hours.

Endoscopic management of foreign bodies in the upper gastrointestinal tract: a retrospective study of 1294 cases.

OBJECTIVE: To report our endoscopic outcomes and explore the effects of duration of impaction and anesthetic methods on the endoscopic removal of foreign bodies in the upper gastrointestinal tract. METHODS: All consecutive patients with suspected foreign body (FB) ingestion between January 2013 and June 2016 were enrolled. Demographic, clinical and endoscopic data were collected and analyzed. RESULTS: A total of 1294 patients aged seven months to 94 years were enrolled. Odynophagia (415 cases, 32.1%), FB sensation (340 cases, 26.3%) and sore throat (267 cases, 20.1%) were the most frequent complaints. The duration of FB impaction ranged from 4 h to over two years. Anatomically, foreign bodies were most commonly located in the esophagus (n = 1025, 86.9%). Bony foreign bodies comprised the majority of identified foreign bodies. The most common underlying pathology was esophageal stricture (38 cases, 53.5%). Nearly half of the patients (49.9%) developed complications. As the duration of impaction increased, the success rate by endoscopy decreased (p < .001), and the complication rate increased (p < .001). Endoscopic management under general anesthesia didn't improve the success rate or lower the complication rate compared with topical pharyngeal anesthesia (p = .793 and p = .085). Age ≥60, duration of impaction longer than one day, impaction in the esophagus, and sharp foreign bodies were identified as risk factors for complications. CONCLUSIONS: Delayed flexible endoscopy in patients, especially elderly patients, with sharp FB impactions in the esophagus results in worse endoscopic outcomes. Endoscopic management under general anesthesia did not improve the therapeutic results compared with topical pharyngeal anesthesia.

Somatostatin regulates NHE8 protein expression via the ERK1/2 MAPK pathway in DSS-induced colitis mice.

Previous studies reported that administration of somatostatin (SST) to human patients mitigated their diarrheal symptoms. Octreotide (an analog of SST) treatment in animals resulted in upregulation of sodium/hydrogen exchanger 8 (NHE8). NHE8 is important for water/sodium absorption in the intestine, and loss of NHE8 function results in mucosal injury. Thus we hypothesized that NHE8 expression is inhibited during colitis and that SST treatment during pathological conditions can restore NHE8 expression. Our data showed for the first time that NHE8 is expressed in the human colonic tissue and that NHE8 expression is decreased in ulcerative colitis (UC) patients. We also found that octreotide could stimulate colonic NHE8 expression in colitic mice. Furthermore, the somatostatin receptor 2 (SSTR2) agonist seglitide and the somatostatin receptor 5 (SSTR5) agonist L-817,818 could restore NHE8 expression via its role in suppressing ERK1/2 phosphorylation. Our study uncovered a novel mechanism of SST stimulation of NHE8 expression in colitis.

Curcumin suppresses 4-hydroxytamoxifen resistance in breast cancer cells by targeting SLUG/Hexokinase 2 pathway.

Triple negative breast cancer (TNBC) is the hardest breast cancer subtype to treat due to lacking therapeutic target and treatment options. In this study, we found that SLUG expression was much higher in TNBC MDA-MB-231 cells than estrogen receptor alpha (ERα) positive breast cancer MCF7 cells. 4-hydroxytamoxifen (4-OHT) promoted SLUG expression, which was blocked by curcumin. Further investigation showed that SLUG activated the transcription of hexokinase-2 (HK2) by binding to HK2 promoter. SLUG knockdown inhibited HK2 expression and weakened 4-OHT resistance of MDA-MB-231 cells. Conversely, SLUG overexpression elevated HK2 level and increased 4-OHT resistance of MCF7 cells. Combination of curcumin and 4-OHT suppressed SLUG and HK2 expression, leading to mitochondrion-mediated apoptosis. These results suggested SLUG as a potential target and curcumin as a promising natural agent for overcoming 4-OHT resistance of TNBC.

Nano-fabrication and related optical properties of InGaN/GaN nanopillars.

Nanopillars with diameters down to 20 nm were fabricated from InGaN/GaN multiple quantum wells (MQWs) by using a nanosphere-SiO2 double mask and inductively coupled plasma (ICP) etching. Clear photoluminescence (PL) signals of the nanopillars were observed at room temperature, and the PL peak energy at 20 K showed a large blueshift of 220 meV compared with that of the original MQWs. The exciton activation energy in the temperature range of 100 ∼ 300 K increased from 33 meV for MQWs to 83 meV for nanopillars. According to the measurements and numerical simulation results, the strain relaxation effect is believed to play a dominant role rather than the quantum confinement effect in determining the emission wavelength of nanopillars. This work also demonstrates a promising method for obtaining III-nitride quantum dots.