Retracted: Arsenic Trioxide Inhibits the Metastasis of Small Cell Lung Cancer by Blocking Calcineurin-Nuclear Factor of Activated T Cells (NFAT) Signaling.

This publication has been retracted by the Editor due to the identification of non-original figure images and manuscript content that raise concerns regarding the credibility and originality of the study. Reference: Jin-Cheng Zheng, Ke-Jie Chang, Yu-Xiang Jin, Xue-Wei Zhao, Bing Li, Meng-Hang Yang. Arsenic Trioxide Inhibits the Metastasis of Small Cell Lung Cancer by Blocking Calcineurin-Nuclear Factor of Activated T Cells (NFAT) Signaling. Med Sci Monit 2019; 25:2228-2237. DOI: 10.12659/MSM.913091.

OrchidBase 5.0: updates of the orchid genome knowledgebase.

Containing the largest number of species, the orchid family provides not only materials for studying plant evolution and environmental adaptation, but economically and culturally important ornamental plants for human society. Previously, we collected genome and transcriptome information of Dendrobium catenatum, Phalaenopsis equestris, and Apostasia shenzhenica which belong to two different subfamilies of Orchidaceae, and developed user-friendly tools to explore the orchid genetic sequences in the OrchidBase 4.0. The OrchidBase 4.0 offers the opportunity for plant science community to compare orchid genomes and transcriptomes and retrieve orchid sequences for further study.In the year 2022, two whole-genome sequences of Orchidoideae species, Platanthera zijinensis and Platanthera guangdongensis, were de novo sequenced, assembled and analyzed. In addition, systemic transcriptomes from these two species were also established. Therefore, we included these datasets to develop the new version of OrchidBase 5.0. In addition, three new functions including synteny, gene order, and miRNA information were also developed for orchid genome comparisons and miRNA characterization.OrchidBase 5.0 extended the genetic information to three orchid subfamilies (including five orchid species) and provided new tools for orchid researchers to analyze orchid genomes and transcriptomes. The online resources can be accessed at https://cosbi.ee.ncku.edu.tw/orchidbase5/.

Arsenic Trioxide Inhibits the Metastasis of Small Cell Lung Cancer by Blocking Calcineurin-Nuclear Factor of Activated T Cells (NFAT) Signaling.

BACKGROUND The inhibitory effect of arsenic trioxide (As2O3) on lung cancer has been reported in some preclinical studies. However, its effect on small cell lung cancer (SCLC) has been poorly explored. Calcineurin and its substrate, nuclear factor of activated T cells (NFAT), mediate the downstream signaling of VEGF, and is critical in the process endothelium activation and tumor metastasis. In this study, we aimed to evaluate whether As2O3 had inhibitory effects on endothelial cells activation and the metastasis of SCLC, and to explore the possible mechanisms. MATERIAL AND METHODS In vitro, human umbilical vein endothelial cells (HUVECs) were used. Cell Counting Kit-8 assay and cell migration assay were performed to determine the effect of As2O3 on HUVECs proliferation and migration. The level of calcineurin, NFAT, downstream factors for Down syndrome candidate region 1 (DSCR1), and the endogenous inhibitor of calcineurin, were evaluated by quantitative PCR and western blotting. In vivo, SCLC metastasis models were established by injecting NCI-H446 cells into tail veins of nude mice. Tumor-bearing mice were treated with As2O3 or calcineurin inhibitor for 10 days, after which tumor metastasis in target organs was evaluated. RESULTS As2O3 significantly inhibited the proliferation and migration of endothelial cells. Also, As2O3 inhibited the expression levels of calcineurin, NFAT, and the downstream target genes CXCR7 and RND1, while it upregulated the level of DSCR1. Both As2O3 and calcineurin inhibitor exhibited notable inhibitory effect on the metastasis of SCLC, without obvious side effects. CONCLUSIONS These findings suggested that As2O3 had remarkable inhibitory effects on the endothelial cell activation and SCLC metastasis, and the mechanism might be related to the blocking of calcineurin-NFAT signaling by upregulating DSCR1.

[Study on the Structural, Optical an Surface Plasmon Characteristics of Mo-Doped ZnO Thin Film].

Mo-doped zinc oxide (ZnO∶Mo) films were deposited with direct current magnetron sputtering on quartz substrates at room temperature. The effects of Mo doping content on the crystal structure, surface microstructure，optical properties and plasmon characteristics of the ZnO films were investigated with X-ray diffraction(XRD),atomic force microscopy (AFM),Spectrophotometer and Raman spectrometer. The XRD pattern reveals that pure ZnO film exhibits good crystallization and c-axis oriented while heavy doping leads to increasing film defects. That results decline the film crystalline quality. When Mo doping content exceeds 3.93 Wt%, the ZnO films transform c-axis oriented into amorphous. The AFM pattern indicates that the surface of amorphous MZO film is extraordinarily flat. The Rq is 498 pm. The transmittance spectra reveal that all samples have an average transmittance of 80% in the visible light range. The optical band gap energy (Eg) increases from 3.28 to 3.60 eV as the Mo doping content increase. The absorbance spectrum indicates that ZnO surface plasmon resonance absorbance perk moves to short-wavelength as the Mo doping content increase. The Raman spectrum suggests that heavy Mo doping make the Raman scattering intensity decrease significantly. This paper obtains amorphous ZnO thin film by Mo doping. That broadens the application field of ZnO thin film materials. Meanwhile, we study the effect of Mo doping concentration on ZnO thin films surface plasmon, which provides important reference value for the preparation of oxidized zinc base photonic devices.

A lysosome-targeting rhodamine fluorescent probe for Cu2+ detection and its applications in test kits and zebrafish imaging.

Tracing copper ions levels in the environment and subcellular microenvironment is crucial due to the key role copper ions play in physiological and pathological processes. Herein, a novel naphthalimide-fused rhodamine probe Rh-Naph-Cu was prepared through modification with phenylhydrazine to produce a closed and non-fluorescent spirolactam. Based on the copper-induced spirolactam ring-opening and hydrolysis process, Rh-Naph-Cu can be employed as a fluorescence off-on probe for copper ions with high selectivity, high sensitivity (limit of detection: 33.0 nM), broad pH-response range (pH: 5.0-10.0), and color change visible with the naked eye. Rh-Nap-Cu could be made into test strips for the in-situ chromogenic detection of Cu2+. Significantly, Rh-Naph-Cu can be utilized for the detection of copper ions in living HeLa cells and zebrafish, and exhibits excellent lysosomal-targeting ability with high Pearson's correlation coefficient (PCC) of 0.96.

Arsenic Trioxide Suppresses Angiogenesis in Non-small Cell Lung Cancer via the Nrf2-IL-33 Signaling Pathway.

BACKGROUND: Non-Small Cell Lung Cancer (NSCLC) ranks as a leading cause of cancer-related mortality, necessitating the urgent search for cost-effective and efficient anti-NSCLC drugs. Our preliminary research has demonstrated that arsenic trioxide (ATO) significantly inhibits NSCLC angiogenesis, exerting anti-tumor effects. In conjunction with existing literature reports, the Nrf2-IL-33 pathway is emerging as a novel mechanism in NSCLC angiogenesis. OBJECTIVE: This study aimed to elucidate whether ATO can inhibit NSCLC angiogenesis through the Nrf2-IL-33 pathway. METHODS: Immunohistochemistry was employed to assess the expression of Nrf2, IL-33, and CD31 in tumor tissues from patients with NSCLC. DETA-NONOate was used as a nitric oxide (NO) donor to mimic high levels of NO in the tumor microenvironment. Western blot, quantitative real-time PCR, and enzyme-linked immunosorbent assay were utilized to evaluate the expression of Nrf2 and IL-33 in the NCI-H1299 cell line. Subcutaneous xenograft models were established in nude mice by implanting NCI-H1299 cells to assess the anti-tumor efficacy of ATO. RESULTS: High expression levels of Nrf2 and IL-33 were observed in tumor samples from patients with NSCLC, and Nrf2 expression positively correlated with microvascular density in NSCLC. In vitro, NO (released from 1mM DETA-NONOate) promoted activation of the Nrf2-IL-33 signaling pathway in NCI-H1299 cells, which was reversed by ATO. Additionally, both Nrf2 deficiency and ATO treatment significantly attenuated NOinduced IL-33 expression. In vivo, both ATO and the Nrf2 inhibitor ML385 demonstrated significant inhibitory effects on angiogenesis tumor growth. CONCLUSION: Nrf2-IL-33 signaling is usually activated in NSCLC and positively correlates with tumor angiogenesis. ATO effectively disrupts the activation of the Nrf2-IL-33 pathway in NSCLC and thus inhibits angiogenesis, suggesting its potential as an anti-angiogenic agent for use in the treatment of NSCLC.

Arsenic trioxide elicits anti-tumor activity by inhibiting polarization of M2-like tumor-associated macrophages via Notch signaling pathway in lung adenocarcinoma.

Drug-resistant advanced lung adenocarcinoma (LUAD) is an aggressive malignancy with limited treatment options. A therapeutic strategy for drug-resistant LUAD is to target the tumor associated macrophages (TAMs), because they play an important role in tumor immune escape, progression and metastasis. In this study, we conducted in vivo and in vitro investigation of the inhibitory effect of arsenic trioxide (ATO) on polarization of TAMs educated by LUAD. We found that ATO at a concentration of 4 µM disrupted the Notch-dependent positive feedback loop between LUAD and TAMs. In this loop, ATO inhibited the expression of Jagged1 and Notch1 in LUAD and suppressed M2 polarization via down-regulating Notch-dependent paracrine of CCL2 and IL1ß. As a result, the secretion of M2-derived TGF-ß1 decreased, thus inducing inhibitions of LUAD proliferation, migration, invasion, colony formation and epithelial-mesenchymal transition. In xenograft mouse models, ATO significantly inhibited tumor growth and down-regulated infiltration of M2-like TAMs in tumor tissues. In clinical LUAD biopsy samples, high Jagged1/Notch1 expression positively correlated with tumor-infiltrated M2-like TAMs, leading to poor prognosis. In conclusion, our results identified a novel tumor immunomodulating function for ATO, which can inhibit the polarization of M2-type TAMs to exert anti-tumor effects in the tumor microenvironment. Our results demonstrated the translational potential of repurposing ATO to target TAMs for lung adenocarcinoma treatment.

A liquid chromatography-tandem mass spectrometry method for simultaneous quantification of thirty-nine tyrosine kinase inhibitors in human plasma.

Currently, the use of targeted drugs such as tyrosine kinase inhibitors (TKIs) plays an important role in clinical therapy. As the number of approved TKIs continues to increase, existing analysis methods will not be able to meet the growing needs, and will hamper the development of therapeutic drug monitoring (TDM) of TKIs. Based on LC-MS/MS technology, this study tends to develop and validate a multi-component analysis method for simultaneous determination of the concentrations of 39 TKIs in plasma. Spiked plasma was blended with isotope labelled internal standards, and injected into the LC-MS/MS system after protein precipitation by acetonitrile. Chromatographic separation was achieved using an ODS-4 column with gradient elution of formic acid/water (1:1000; v/v) and acetonitrile. Analytes detection was conducted in positive ionisation mode using MRM. The total run time was 8 min. The method validation was conducted by assessing the following parameters: selectivity, linearity and the lower limit of qualification, accuracy and precision, stability, matrix effect and recovery. The concentrations of 39 TKIs showed good linearity within the range of their respective standard curves in plasma, the accuracy of all quality control samples ranged from 85.9% to 114.1%, and the precision was lower than 13.3%. The extraction recovery ranged from 92.6% to 114.7%, and the matrix effect of plasma was lower than 11.3%. This new method was successfully developed, can be used for the determination of drug concentrations in multiple patients with different kinds of TKIs, and will therefore be suitable for TDM of 39 TKIs.

MDM2-mediated Inhibitory Effect of Arsenic Trioxide on Small Cell Lung Cancer Cell Line by Degrading Mutant p53.

INTRODUCTION: Small cell lung cancer (SCLC) is featured by a high TP53 mutant rate. Our previous research found that arsenic trioxide (As2O3) could significantly inhibit the growth and metastasis of SCLC. Studies have shown that the degradation of mutant p53 mediated by murine double minute 2 (MDM2) can be induced by As2O3, which probably contributes to the inhibition of SCLC, but the detailed mechanism is still unclear. We aimed to testify that As2O3 can inhibit the growth of SCLC cells by degrading mutant p53 protein via binding to MDM2. METHODS: CCK-8 assay, cell cycle analysis, and western blot of apoptosis markers were used to evaluate the inhibitory effect of As2O3 on NCI-H446 cells (containing mutant p53) and NCI-H1299 cells (p53 null). The effects of As2O3 on p53 and its downstream proteins were identified by western blot using mut-p53-knockdown and overexpressed cell models. MDM2-knockdown cell models were constructed, and western blot, co-IP of mut-p53, and ubiquitin were carried out to explore the mediating effect of MDM2 in As2O3 induced mut-p53 degradation. RESULTS: As2O3 inhibited proliferation and induced cell cycle arrest and apoptosis of SCLC cells in a dose- and timedependent manner. After mut-p53 knockdown or overexpressed, the inhibitory effect of As2O3 was dampened or enhanced. Additionally, As2O3-induced mut-p53 ubiquitination was significantly weakened after MDM2 knockdown. CONCLUSION: As2O3 could inhibit SCLC cells by inhibiting proliferation and inducing cell cycle arrest and apoptosis. These inhibitory effects were achieved at least in part by upregulating MDM2, which, in turn, promotes ubiquitination and degradation of mut-p53.

Diploid and tetraploid genomes of Acorus and the evolution of monocots.

Monocots are a major taxon within flowering plants, have unique morphological traits, and show an extraordinary diversity in lifestyle. To improve our understanding of monocot origin and evolution, we generate chromosome-level reference genomes of the diploid Acorus gramineus and the tetraploid Ac. calamus, the only two accepted species from the family Acoraceae, which form a sister lineage to all other monocots. Comparing the genomes of Ac. gramineus and Ac. calamus, we suggest that Ac. gramineus is not a potential diploid progenitor of Ac. calamus, and Ac. calamus is an allotetraploid with two subgenomes A, and B, presenting asymmetric evolution and B subgenome dominance. Both the diploid genome of Ac. gramineus and the subgenomes A and B of Ac. calamus show clear evidence of whole-genome duplication (WGD), but Acoraceae does not seem to share an older WGD that is shared by most other monocots. We reconstruct an ancestral monocot karyotype and gene toolkit, and discuss scenarios that explain the complex history of the Acorus genome. Our analyses show that the ancestors of monocots exhibit mosaic genomic features, likely important for that appeared in early monocot evolution, providing fundamental insights into the origin, evolution, and diversification of monocots.

Arsenic Trioxide Restrains Lung Cancer Growth and Metastasis by Blocking the Calcineurin-NFAT Pathway by Upregulating DSCR1.

BACKGROUND: Anti-angiogenesis therapy mostly aimed at targeting vascular endothelial growth factor (VEGF) and its receptors have been widely applied to lung cancer. However, the improvement in the patient's overall survival remains dissatisfying. Previously, we demonstrated that arsenic trioxide (As2O3) exerts an anti-lung cancer effect through anti-angiogenesis, but the details of the mechanism in play remain unclear. Herein, we focused on the calcineurin-NFAT pathway, downstream of VEGF, and its endogenous inhibitor DSCR1. OBJECTIVE: To demonstrate the mechanism of As2O3 restraining lung cancer growth and metastasis by blocking the calcineurin-NFAT pathway by upregulating DSCR1. METHODS: We constructed xenografts and metastasis models based on wild-type (WT) and DSCR1 knockout (DSCR1-/-) mice, and carried out qPCR, Western blot, immunohistochemistry, in vivo imaging and calculated microvessel density to evaluate the effects of As2O3 on angiogenesis, tumor growth, metastasis, and the protein expression levels of DSCR1 and calcineurin-NFAT pathway-related molecules. RESULTS: As2O3 inhibited tumor growth and metastasis, reduced microvessel formation, and induced vascular lumen malformation in WT mice. At the protein level, As2O3 upregulated DSCR1, downregulated NFAT2 and its downstream molecules, but had no effect on calcineurin A. However, in DSCR1-/- mice, the above-mentioned effects of As2O3 were abolished. CONCLUSION: As2O3 can suppress lung cancer growth and metastasis through anti-angiogenesis effects by blocking the calcineurin-NFAT pathway by upregulating DSCR1. The results shed light on the antitumor mechanism of As2O3 and are a step forward in the identification of As2O3 as a new drug in the treatment of lung cancer.

Advances and prospects of orchid research and industrialization.

Orchidaceae is one of the largest, most diverse families in angiosperms with significant ecological and economical values. Orchids have long fascinated scientists by their complex life histories, exquisite floral morphology and pollination syndromes that exhibit exclusive specializations, more than any other plants on Earth. These intrinsic factors together with human influences also make it a keystone group in biodiversity conservation. The advent of sequencing technologies and transgenic techniques represents a quantum leap in orchid research, enabling molecular approaches to be employed to resolve the historically interesting puzzles in orchid basic and applied biology. To date, 16 different orchid genomes covering four subfamilies (Apostasioideae, Vanilloideae, Epidendroideae, and Orchidoideae) have been released. These genome projects have given rise to massive data that greatly empowers the studies pertaining to key innovations and evolutionary mechanisms for the breadth of orchid species. The extensive exploration of transcriptomics, comparative genomics, and recent advances in gene engineering have linked important traits of orchids with a multiplicity of gene families and their regulating networks, providing great potential for genetic enhancement and improvement. In this review, we summarize the progress and achievement in fundamental research and industrialized application of orchids with a particular focus on molecular tools, and make future prospects of orchid molecular breeding and post-genomic research, providing a comprehensive assemblage of state of the art knowledge in orchid research and industrialization.

Interstitial lung diseases after leflunomide use in nephropathy: an analysis of reported cases in Chinese literature.

BACKGROUND: Leflunomide (LEF)-induced interstitial lung disease (ILD) has been reported in patients with rheumatoid arthritis. In China, LEF is used off-label for the treatment of nephropathy. METHODS: Systemic review of the Chinese literature from 1999 to June 2010 for case reports and case series of LEF-induced ILD in nephropathy patients. RESULTS: We identified seven cases of LEF-induced ILD (three males and four females), with an average age of 45.9 years (range: 9-69 years). Six cases had primary nephrotic syndrome and one had Henoch-Schoenlein purpura. Four cases had diagnoses of renal pathology. Five patients were given loading doses of LEF, followed by a maintenance dose of 10-30 mg/day. The mean duration of LEF use was 62.9 ± 33.0 days (range: 20-120 days). The mean accumulated dose of LEF was 1192.5 mg (range: 830-1800 mg). LEF therapy was considered effective in four patients. Four patients died (57.1%), three of whom had developed fevers. All three male patients died and both of the young patients died. The mean duration of LEF treatment was 83 days for patients who died and 37 days for survivors. CONCLUSIONS: LEF-induced ILD in patients with nephropathy usually occurred after ∼2 months of treatment and an accumulated dose of 1192.5 mg. Duration of LEF use, male sex, young age and fever seemed to increase the risk of mortality.

Insights into the Effect of Reactive Oxygen Species Regulation on Photocatalytic Performance via Construction of a Metal-Semiconductor Heterojunction.

Reactive oxygen species (ROS), as primary intermediates formed during photocatalytic reactions, are critical for a photocatalyst to realize high activity. The major objective of this study was to investigate the regulation of ROS involved in the photocatalytic degradation process via constructing a typical metal-semiconductor hybrid heterojunction using Ag nanoparticles/anatase TiO2 as an example. Based on radical capturing, electron paramagnetic resonance, and electron spin resonance experiments, an increase in the available ROS can be achieved in the Ag/TiO2 heterojunction due to the fast separation of photogenerated carriers. In addition, due to the change in the electron transfer pathway, superoxide radicals (·O-2) are the dominant reactive species responsible for dye degradation using Ag/TiO2 rather than hydroxyl radicals (·OH) as the main free radicals in pristine TiO2. This study offers fresh insight into the regulation of ROS in photodegradation via the construction of a Ag/TiO2 heterojunction.

[Biological Ultra-weak Luminescence and Its Application to Research of Acupuncture].

Ultra-weak bioluminescence (UWL) is a physiological phenomenon widely existing in all the biological activities including human, animals, plants, etc., which reflects the energy metabolism of the organism. Since the last century, ultra-weak photon emission (UPE) has been applied to the study of the essence of meridians and acupoints of traditional Chinese medicine and obtained some results as the higher luminescence characteristics, but many problems remain unsolved due to the limitation of detection technology. In recent years, along with the development of bioluminescence signal acquiring system and imaging system, we are able to further explore the characteristics and biological mechanisms of UWL of acupuncture points and meridians in the human body. We proposed to study changes of ultra-weak luminous intensity of acupuncture points and meridians before and after needling stimulation, and the delayed effect of UPE phenomenon, etc., trying to reveal their regularities and essence. In this paper, the prospect of application of UPE to acupuncture research is also discussed by combining newly acquired results of some biological substances of acupoints in experimental studies.

Anti-angiogenic effect of arsenic trioxide in lung cancer via inhibition of endothelial cell migration, proliferation and tube formation.

Arsenic trioxide (As2O3) exhibits a remarkable effect on leukemia treatment; however, its effect on solid tumors remains poorly explored. The present study demonstrated the inhibitory effect of As2O3 on lung cancer and explored its possible mechanism. It was observed that As2O3 significantly inhibited the growth of lung cancer xenografts and tumor angiogenesis in vivo. The inhibitory effect of As2O3 on cell proliferation in vitro was more remarkable in vascular endothelial cells than in lung cancer cells. It was also observed that As2O3 inhibited the migration of vascular endothelial cells and disrupted vascular tube formation on Matrigel assays. In addition, a series of key signaling factors involved in multiple stages of angiogenesis, including matrix metalloproteinase (MMP)-2, MMP-9, platelet-derived growth factor (PDGF)-BB/PDGF receptor-ß, vascular endothelial growth factor (VEGF)-A/VEGF receptor-2, basic fibroblast growth factor (FGF)/FGF receptor-1 and delta like canonical Notch ligand 4/Notch-1, were regulated by As2O3. These findings suggested that anti-angiogenesis may be an underlying mechanism of As2O3 anticancer activity in lung cancer.

[Experimental study of degradable chitin long fiber reinforced polycaprolactone for reconstruction of chest wall defects].

OBJECTIVE: To investigate the application of a novel degradable biomaterial as a chest wall prosthesis and provide valuable scientific basis for clinical application. METHODS: Preparation of chitin long fiber reinforced polycaprolactone (PCL) by means of melt blending and modeling. Full-thickness chest wall defects of 10 cm x 8 cm was created in 10 dogs and then repaired with long chitin fiber reinforced PCL artificial rib in 8 dogs (tested group) and Marlex mesh in 2 dogs (control group). It was dynamically observed that the situation of the implanted chest wall prosthesis and the progress of the regeneration of the chest wall tissue postoperatively. RESULTS: No operative and perioperative deaths were observed in all experimental dogs. In tested group, slight paradoxical respiration occurred in 2 dogs and could not be seen in 2 weeks. No chest wall subsidence and infection occurred. New bone tissue obviously regenerated around both resection ends of the ribs and integrated tightly with artificial ribs. In control group, there were evidently paradoxical respiration and chest wall subsidence. Marlex mesh folded and was enveloped by fibrous tissue. CONCLUSION: Degradable chitin long fiber reinforced PCL can provide effective support to chest walls and is a practicable material for chest wall reconstruction.

Two new ursane-type triterpenoid saponins from Elsholtzia bodinieri.

Two new ursane-type triterpenoid saponins, bodiniosides M (1) and N (2), along with three known saponins, oblonganosides I (3), pseudobuxussaponin B (4) and bodinioside A (5), were isolated from the aerial parts of Elsholtzia bodinieri. The structures of compounds 1 and 2 were characterized by spectroscopic data as well as acid hydrolysis and GC analysis as 3-O-ß-D-xylopyranosyl-19α-hydroxy-23-acetoxy-urs-12(13)-en-28-oic acid 28-O-α-L-rhamnopyranosyl-(1-2)-ß-D-glucopyranoside and 3-O-ß-D-glucopyranosyl-2α,19α-dihydroxy-urs-12(13)-en-28,20ß-lactone. Compounds 1 and 5 exhibited potent anti-HCV activities in vitro with a selective index of 6.53 and 4.41, respectively.

Laparoscopic Complete Mesocolic Excision for Stage II/III Left-Sided Colon Cancers: A Prospective Study and Comparison with D3 Lymph Node Dissection.

BACKGROUND: To investigate the similarities and differences of laparoscopic complete mesocolic excision (CME) to a colon resection with a D3 lymphadenectomy for the stage II/III left-sided colon carcinoma. METHODS: Patients between July 2011 and August 2014 were randomized into D3 and CME groups. Mesenteric area, log odds of positive lymph nodes (LODDS), and other operative parameters were collected and assessed. RESULTS: The average specimen sizes were 5730 ± 828 mm(2) in superior rectal artery (SRA)-preserving D3, 8145 ± 1022 mm(2) in SRA-nonpreserving D3, and 8745 ± 1039 mm(2) in the CME group; the differences were significant (P < .0001). The number of lymph nodes collected from CME specimens was larger, but the CME specimens did not contain an elevated value of LODDS or positive nodes or lymph node ratio (LNR). There were also no significant differences between recovery times of bowel function. Although it took more operation time in D3 approach, especially in SRA-preserving D3 operation, the difference was not significant. Concerning the leakage rate (P = .34) and vessel-related complications (P = .64), there were no significant differences either. CONCLUSIONS: Both standard D3 resection and CME could achieve a high quality of mesocolic plane grade for stage II/III colon cancer. The LODDS and LNR were comparable, and those were not relevant to mesenteric size.

Efficacy of Arsenic Trioxide in the Treatment of Malignant Pleural Effusion Caused by Pleural Metastasis of Lung Cancer.

The aim of the study was to investigate the mechanism of arsenic trioxide (As2O3) in the treatment of malignant pleural effusion (MPE) caused by pleural metastasis of lung cancer. A mouse model of MPE caused by pleural metastasis of lung cancer was first established, and As2O3 was then intraperitoneally injected to treat the MPE. Mice treated with bevacizumab and bleomycin were included as positive controls, and placebo equivalents were also used as negative controls. The effects of As2O3 on MPE volume, pleural vessel density, vascular permeability, expression of angiogenic function-related factors, including vascular endothelial growth factor (VEGF) and tumor necrosis factor alpha (TNF-α), as well as nuclear factor-κB (NF-κB) activity in pleural carcinomatosis, were observed. Intraperitoneal injection of As2O3 reduced the volume of MPE and decreased vascular density and permeability in pleural metastatic nodules in a dose-dependent manner. Moreover, dose-dependent decreases in VEGF and TNF-α expression in MPE, and NF-κB activity in pleural carcinomatosis, were also found after As2O3 treatment. We showed that As2O3 can down-regulate VEGF expression via inhibition of NF-κB, and decrease vascular density and permeability in pleural metastatic nodules, thereby eliciting its effects on MPE caused by pleural metastasis of lung cancer. Our results provide a foundation for an As2O3-based clinical treatment program.