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Negative correlation between lncRNA-TTN-AS1 and miR-133b in ESCC tissues and cell lines.

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Purpose: Emerging studies demonstrate that long noncoding RNAs (lncRNA) participate in the regulation of various cancers. In the current study, a novel lncRNA-TTN-AS1 has been identified and explored in esophageal squamous cell carcinoma (ESCC).Experimental Design: To discover a new regulatory circuitry in which RNAs crosstalk with each other, the transcriptome of lncRNA-miRNA-mRNA from ESCC and adjacent nonmalignant specimens were analyzed using multiple microarrays and diverse bioinformatics platforms. The functional role and mechanism of a novel lncRNA-TTN-AS1 were further investigated by gain-of-function and loss-of-function assays in vivo and in vitro. An ESCC biomarker panel, consisting of lncRNA-TTN-AS1, miR-133b, and FSCN1, was validated by qRT-PCR and in situ hybridization using samples from 148 patients.Results: lncRNA-TTN-AS1 as an oncogene is highly expressed in ESCC tissues and cell lines, and promotes ESCC cell proliferation and metastasis. Mechanistically, lncRNA-TTN-AS1 promotes expression of transcription factor Snail1 by competitively binding miR-133b, resulting in the epithelial–mesenchymal transition (EMT) cascade. Moreover, lncRNA-TTN-AS1 also induces FSCN1 expression by sponging miR-133b and upregulation of mRNA-stabilizing protein HuR, which further promotes ESCC invasion cascades. We also discovered and validated a clinically applicable ESCC biomarker panel, consisting of lncRNA-TTN-AS1, miR-133b, and FSCN1, that is significantly associated with overall survival and provides additional prognostic evidence for ESCC patients.Conclusions: As a novel regulator, lncRNA-TTN-AS1 plays an important role in ESCC cell proliferation and metastasis. The lncRNA-TTN-AS1/miR133b/FSCN1 regulatory axis provides bona fide targets for anti-ESCC therapies. Clin Cancer Res; 24(2); 486–98. ©2017 AACR.

SET is a multifunctional histone-binding oncoprotein that regulates transcription by an unclear mechanism. Here we show that SET enhances estrogen-dependent transcription. SET knockdown abrogates transcription of estrogen-responsive genes and their enhancer RNAs. In response to 17β-estradiol (E2), SET binds to the estrogen receptor α (ERα) and is recruited to ERα-bound enhancers and promoters at estrogen response elements (EREs). SET functions as a histone H2 chaperone that dynamically associates with H2A.Z via its acidic C-terminal domain and promotes H2A.Z incorporation, ERα, MLL1, and KDM3A loading and modulates histone methylation at EREs. SET depletion diminishes recruitment of condensin complexes to EREs and impairs E2-dependent enhancer-promoter looping. Thus, SET boosts E2-induced gene expression by establishing an active chromatin structure at ERα-bound enhancers and promoters, which is essential for transcriptional activation.

SETβ is the predominant isoform of oncoprotein SE translocation (SET) in various breast cancer cell lines. Interactome-transcriptome analysis has shown that SETβ is intimately associated with cellular stress response. Among various exogenous stimuli, formaldehyde (FA) causes distinct biological effects in a dose-dependent manner. In response to FA at different concentrations, SET dynamically shuttles between the nucleus and cytoplasm, performing diverse biofunctions to restore homeostasis. At a low concentration, FA acts as an epidermal growth factor (EGF) and activates the HER2 receptor and downstream signaling pathways in HER2

Sparse additive machines (SAMs) have attracted increasing attention in high dimensional classification due to their representation flexibility and interpretability. However, most of existing methods are formulated under Tikhonov regularization scheme with the hinge loss, which are susceptible to outliers. To circumvent this problem, we propose a sparse additive machine with ramp loss (called ramp-SAM) to tackle classification and variable selection simultaneously. Misclassification error bound is established for ramp-SAM with the help of detailed error decomposition and constructive hypothesis error analysis. To solve the nonsmooth and nonconvex ramp-SAM, a proximal block coordinate descent method is presented with convergence guarantees. The empirical effectiveness of our model is confirmed on simulated and benchmark datasets.

B cell dysfunction due to obesity can be associated with alterations in the levels of micro-RNAs (miRNAs). However, the role of miRNAs in these processes remains elusive. Here, we show that miR-802 is increased in the pancreatic islets of obese mouse models and demonstrate that inducible transgenic overexpression of miR-802 in mice causes impaired insulin transcription and secretion. We identify Foxo1 as a transcription factor of miR-802 promoting its transcription, and NeuroD1 and Fzd5 as targets of miR-802-dependent silencing. Repression of NeuroD1 in β cell and primary islets impairs insulin transcription and reduction of Fzd5 in β cell, which, in turn, impairs Ca2+ signaling, thereby repressing calcium influx and decreasing insulin secretion. We functionally create a novel network between obesity and β cell dysfunction via miR-802 regulation. Elucidation of the impact of obesity on microRNA expression can broaden our understanding of pathophysiological development of diabetes., Obesity predisposes to type 2 diabetes, but the mechanisms of obesity-associated β cell dysfunction are incompletely understood. Here the authors report that obesity increases the levels of miR-802, which impairs insulin transcription and secretion by targeting NeuroD1 and Fzd5.

In recent years, sparse additive machines have attracted increasing attention in high dimensional classification due to their flexibility and representation interpretability. However, most of the existing methods are formulated under Tikhonov regularization schemes associated with the hinge loss, where the distribution information of observations is neglected usually. To circumvent this problem, we propose an optimal margin distribution additive machine (called ODAM) by incorporating the optimal margin distribution strategy into sparse additive models. The proposed approach can be implemented by a dual coordinate descent algorithm and its empirical effectiveness is confirmed on simulated and benchmark datasets.

DNA repair machinery is involved in estrogen-dependent transactivation. Mounting evidence suggests that mechanisms underlying estrogen-induced DNA damage are complicated. To date estrogen-induced DNA oxidation and its impact on ERα-mediated transaction remains ambiguous. Herein, we found that the process of 17β-estradiol (E2)-induced ROS production can be approximately divided into two phases according to responding time and generation mechanisms. The intracellular Ca

Tumor-associated macrophages (TAMs) are one of the main cellular components in the tumor microenvironment (TME). In many types of solid tumors, TAMs tend to accumulate in hypoxic areas and are intimately related to poor patient prognosis. However, the underlying mechanisms by which TAMs infiltrate hypoxic tumor regions remain unclear. In this study, we report that genetic deletion of SE translocation (SET) in myeloid cells inhibited the entry of TAMs into the hypoxic tumor region and abated their proangiogenic and immunosuppressive functions, ultimately inhibiting tumor growth. Mechanistically, in response to hypoxic tumor supernatant stimulation, SET in macrophages shuttled between the nucleus and cytoplasm via the PKC-CK2α signaling axis. Cytoplasmic retention of SET increased ERK and P38 signaling by inhibiting PP2A, which promoted TAM migration into the hypoxic area and polarization toward the M2 phenotype. Therefore, we conclude that SET modulates tumor immunity by acting as a key regulator of macrophage positioning and function in the tumor.

TPS488 Background: About 30.3-58.0% of patients who undergo esophagectomy may experience recurrence. The efficacy of postoperative chemoradiation has not been demonstrated in a randomized trial in patients with esophageal squamous cell carcinoma (ESCC) compared to surgery along. Therefore, it is urgent to explore more effective and safer postoperative regimen for resectable ESCC. Checkmate 577 has demonstrated immunotherapy can prolong disease free survival (DFS) for patients who have residual disease following preoperative chemoradiation and R0 resection. Anlotinib is an orally administered tyrosine kinase inhibitor that targets VEGFR1-3, FGFR1-4 and PDGFRα/β. In a randomized, double-blind phase 2 trial, the use of anlotinib in previously treated metastatic ESCC patients significantly improved progression-free survival (PFS) compared with placebo ( NCT02649361 ). TQB2450 is a novel humanized monoclonal antibody against PD-L1, which has shown encouraging activity in combination with anlotinib in the treatment of multiple tumors, such as biliary tract cancer (NCT03996408) and ovarian cancer (NCT04236362). The ALTER-E005 study is designed to evaluate the efficacy and safety of anlotinib combined with TQB2450as adjuvant therapy in ESCC patients. Methods: ALTER-E005 is a multi-center, single-arm, phase II study. A total of 30 patients will be enrolled. Eligible pts (≥18 years) must be histologically confirmed T1-2N1-3M0 or T3-4NanyM0 ESCC; received radical (R0) resection of ESCC with no recurrence in imaging examination within 6-12 weeks after surgery; ECOG PS 0–1. Patients enrolled will receive oral anlotinib 12 mg on days 1-14 and intravenous TQB2450 1,200 mg on day 1 every 3 weeks until disease recurrence. The primary endpoint is DFS. The secondary endpoints include safety, 1-year DFS rate, 3-year DFS rate, 1-year overall survival (OS) rate, and 3-year OS rate. Enrollment to the ALTER-E005 trial is currently ongoing in China. Clinical trial information: NCT05252078 .

The tumor microenvironment (TME) is jointly constructed by a variety of cell types, including tumor cells, immune cells, fibroblasts, and epithelial cells, among others. The cells within the TME interact with each other and with tumor cells to influence tumor development and progression. As the most abundant immune cells in the TME, macrophages regulate the immune network by not only secreting a large amount of versatile cytokines but also expressing a series of ligands or receptors on the surface to interact with other cells directly. Due to their strong plasticity, they exert both immunostimulatory and immunosuppressive effects in the complex TME. The major effector cells of the immune system that directly target cancer cells include but are not limited to natural killer cells (NKs), dendritic cells (DCs), macrophages, polymorphonuclear leukocytes, mast cells, and cytotoxic T lymphocytes (CTLs). Among them, NK cells are the predominant innate lymphocyte subsets that mediate antitumor and antiviral responses. The activation and inhibition of NK cells are regulated by cytokines and the balance between activating and inhibitory receptors. There is an inextricable regulatory relationship between macrophages and NK cells. Herein, we systematically elaborate on the regulatory network between macrophages and NK cells through soluble mediator crosstalk and cell-to-cell interactions. We believe that a better understanding of the crosstalk between macrophages and NKs in the TME will benefit the development of novel macrophage- or NK cell-focused therapeutic strategies with superior efficacies in cancer therapy.

To achieve synergistic photodynamic–photothermic therapy, we fabricate the novel phycocyanin (PC)-functionalized black phosphorus quantum dots (BPQDs) referred as PC@BPQDs through a one-step stirring method. PC@BPQDs are characterized by the feature of possessing both near-infrared (NIR) induced photothermal and photodynamic activity. The PC layer not only effectively alleviates plasma protein adsorption onto BPQDs, but also functionally boosts the photothermal therapy efficiency by enhanced ROS release, resulting in increased apoptosis in vitro. Moreover, PC@BPQDs eradicate tumors with high efficacy and low toxicity in vivo. Thus, PC@BPQDs have a promising potential in future therapeutic implications.

Restoring β-cell mass by the transplantation of pancreatic islets is an effective diabetes treatment, but it is limited by the shortage of donor organs. CD133-expressing pancreatic ductal epithelial cells (PDECs) have the ability to generate insulin-producing cells. The expansion of these cells is dependent on extrinsic niche factors, but few of those signals have been identified. In this study, CD133-expressing PDECs were purified by sorting from adult wild-type C57BL/6 mice and TGFβRII

Background: Breast cancer stem cells (BCSCs) play an essential role in facilitating breast cancer relapse and metastasis. The underlying mechanism, however, remains incompletely understood. In the current study, we investigated the clinical significance, biological function and mechanism of a long noncoding RNA CCAT1 (LncCCAT1) in BCSCs. Methods: Firstly, lncRNAs expression in poorly differentiated breast cancer tissues and BCSCs were measured by lncRNA microarray and confirmed in breast cancer tissues and cell lines. The functional roles and mechanisms of LncCCAT1 were further investigated by gain and loss of function assays in vitro and in vivo. Results: LncCCAT1 is markedly upregulated in breast cancer tissues BCSCs and is correlated with poor outcomes in breast cancer patients. Overexpression of LncCCAT1 contributes to the proliferation, stemness, migration and invasion capacities of BCSCs. Mechanistic investigation suggests that LncCCAT1 can interact with miR-204/211, miR-148a/152 and Annexin A2(ANXA2), then upregulate T-cell factor 4 (TCF4) or promote translocation of β-catenin to the nucleus where it activates TCF4, leading to the activation of wingless/integrated (Wnt) signaling. Furthermore, TCF4 can also bind to the promoter of LncCCAT1 to promote LncCCAT1 transcription, thus forming a positive feedback regulatory circuit of LncCCAT1-TCF4-LncCCAT1 in BCSCs. Conclusions: LncCCAT1 plays an important role in breast cancer progression and may serve as a novel target for breast cancer diagnosis and therapy.

Background: Little is known about the incidence of ipilimumab-related serious adverse events (SAEs) across various tumor types, drug doses and treatment regimens. Methods: PubMed database was searched up to November, 2017 to identify prospective clinical trials of ipilimumab therapy for adult patients with cancer. Comparisons of the incidence were based on the χ2 test in univariate analysis and the logistic regression model in multivariate analysis. Results: Twenty-four studies (4549 patients) with 35 independent study cohorts (21 melanoma, 6 prostate cancer, 5 NSCLC, and 3 SCLC cohorts) of ipilimumab were included in the meta-analysis. The overall incidence of SAEs during ipilimumab mono-therapy was 26.1% (95% CI, 21.1%-31.8%). SAEs were more frequent in the 10 mg/kg groups than in the 3 mg/kg groups (35.9% vs 17.3%; P < 0.001). Combination therapy showed significantly higher incidence than mono-therapy in melanoma (33.8% vs 25.0%; P = 0.002). After adjustment for potential confounders, multivariable analyses demonstrated lower odds of SAEs in NSCLC (odds ratio [OR] 0.52, 95% CI 0.40-0.69, P < 0.001) and SCLC (OR 0.41, 95% CI 0.31-0.54, P < 0.001) compared with melanoma. The 10mg/kg cohort presented significantly higher odds than the 3mg/kg (OR 2.84, 95% CI 2.35-3.43, P < 0.001). The combination therapy showed significantly higher odds than the mono-therapy (OR 1.38, 95% CI 1.11-1.71, P = 0.003). Conclusions: The incidence of ipilimumab-related SAEs was higher in melanoma, the 10mg/kg group and during combination therapy. Clinicians should enhance awareness of these risk factors in clinical practice and carefully monitor patients.

Background At present, the gastric tube is the first choice for esophageal reconstruction after esophagectomy for various benign and malignant diseases. However, when the stomach is not available, a pedicled jejunum or colon is used to reconstruct the esophagus. The present study aimed to compare the postoperative outcomes and quality of life of patients receiving jejunal and colonic conduits. Methods In the present retrospective study, the clinical data of 71 patients with esophageal carcinoma, who received jejunal reconstruction (jejunum group, n = 34) and colonic reconstruction (colon group, n = 37) from 2005 to 2015, were compared. Results Compared with the colon group, the jejunum group had a lower incidence of postoperative anastomotic leakage, lesser duration of postoperative drainage, and faster recovery. Furthermore, the scores were better in the jejunum group than in the colon group, in terms of short-term overall quality of life, physical function and social relationships. Moreover, the jejunal group had a significantly lower frequency of pH 5 min (N45) and the longest reflux time (LT) at 24 weeks after surgery. Conclusion In esophageal cancer, when gastric tube construction is not feasible, a pedicled jejunum may be preferred over a colonic conduit due to lower incidence of acid reflux, anastomotic leakage and higher postoperative short-term quality of life, and rapid postoperative recovery.

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As a class of endogenous noncoding RNAs, circular RNAs (circRNAs) have been recently identified to regulate tumourigenesis and progression in multiple malignancies. However, the expression profiles and function of circRNAs in breast cancer metastasis are largely unknown. Here, we determined that the expression of a novel circRNA, which we named circIRAK3, was increased in metastatic breast cancer (BC) cells and predictive of BC recurrence. Gain-of-function and loss-of-function studies in BC cells demonstrated that circIRAK3 promoted cell migration, invasion and metastasis in vitro and in vivo but did not affect cell proliferation, colony formation or cell cycle progression. Using circIRAK3 in vivo precipitation and luciferase reporter assays, we identified miR-3607 as a circIRAK3-associated miRNA. Furthermore, RNA sequencing and bioinformatics analysis showed that forkhead box C1 (FOXC1), the target of miR-3607, was downregulated in circIRAK3-silenced cells and mediated circIRAK3-induced BC cell migration. Intriguingly, FOXC1 could, in turn, bind to the IRAK3 promoter, triggering a positive-feedback loop that perpetuated the circIRAK3/miR-3607/FOXC1 signaling axis. Collectively, our findings indicated that circIRAK3 may exert regulatory roles in BC metastasis and may be a potential target for metastatic BC therapy.

Purpose: Emerging studies demonstrate that long noncoding RNAs (lncRNA) participate in the regulation of various cancers. In the current study, a novel lncRNA-TTN-AS1 has been identified and explored in esophageal squamous cell carcinoma (ESCC). Experimental Design: To discover a new regulatory circuitry in which RNAs crosstalk with each other, the transcriptome of lncRNA-miRNA-mRNA from ESCC and adjacent nonmalignant specimens were analyzed using multiple microarrays and diverse bioinformatics platforms. The functional role and mechanism of a novel lncRNA-TTN-AS1 were further investigated by gain-of-function and loss-of-function assays in vivo and in vitro. An ESCC biomarker panel, consisting of lncRNA-TTN-AS1, miR-133b, and FSCN1, was validated by qRT-PCR and in situ hybridization using samples from 148 patients. Results: lncRNA-TTN-AS1 as an oncogene is highly expressed in ESCC tissues and cell lines, and promotes ESCC cell proliferation and metastasis. Mechanistically, lncRNA-TTN-AS1 promotes expression of transcription factor Snail1 by competitively binding miR-133b, resulting in the epithelial–mesenchymal transition (EMT) cascade. Moreover, lncRNA-TTN-AS1 also induces FSCN1 expression by sponging miR-133b and upregulation of mRNA-stabilizing protein HuR, which further promotes ESCC invasion cascades. We also discovered and validated a clinically applicable ESCC biomarker panel, consisting of lncRNA-TTN-AS1, miR-133b, and FSCN1, that is significantly associated with overall survival and provides additional prognostic evidence for ESCC patients. Conclusions: As a novel regulator, lncRNA-TTN-AS1 plays an important role in ESCC cell proliferation and metastasis. The lncRNA-TTN-AS1/miR133b/FSCN1 regulatory axis provides bona fide targets for anti-ESCC therapies. Clin Cancer Res; 24(2); 486–98. ©2017 AACR.

Model-free variable selection has attracted increasing interest recently due to its flexibility in algorithmic design and outstanding performance in real-world applications. However, most of the existing statistical methods are formulated under the mean square error (MSE) criterion, and susceptible to non-Gaussian noise and outliers. As the MSE criterion requires the data to satisfy Gaussian noise condition, it potentially hampers the effectiveness of model-free methods in complex circumstances. To circumvent this issue, we present a new model-free variable selection algorithm by integrating kernel modal regression and gradient-based variable identification together. The derived modal regression estimator is related closely to information theoretic learning under the maximum correntropy criterion, and assures algorithmic robustness to complex noise by replacing learning of the conditional mean with the conditional mode. The gradient information of estimator offers a model-free metric to screen the key variables. In theory, we investigate the theoretical foundations of our new model on generalization-bound and variable selection consistency. In applications, the effectiveness of the proposed method is verified by data experiments.

Breast cancer is the most prevalent cancer in women worldwide, which remains incurable once metastatic. Breast cancer stem cells (BCSCs) are a small subset of breast cancer cells which are essential in tumor formation, metastasis, and drug resistance. microRNAs (miRNAs) play important roles in the breast cancer cells and BCSCs by regulating specific genes. In this study, we found that miR-29a was up-regulated in BCSCs, in aggressive breast cancer cell line and in breast cancer tissues. We also confirmed suppressor of variegation 4–20 homolog 2 (SUV420H2), which is a histone methyltransferase that specifically trimethylates Lys-20 of histone H4 (H4K20), as the target of miR-29a. Both miR-29a overexpression and SUV420H2 knockdown in breast cancer cells promoted their migration and invasion in vitro and in vivo. Furthermore, we discovered that SUV420H2-targeting miR-29a attenuated the repression of connective tissue growth factor (CTGF) and growth response protein-1 (EGR1) by H4K20 trimethylation and promoted the EMT progress of breast cancer cells. Taken together, our findings reveal that miR-29a plays critical roles in the EMT and metastasis of breast cancer cells through targeting SUV420H2. These findings may provide new insights into novel molecular therapeutic targets for breast cancer.

Metastasis is one of the leading causes of mortality in cancer patients. As the firstly identified metastasis suppressor, NM23-H1 has been endowed with expectation as a potent target in metastatic cancer therapy during the past decades. However, many challenges impede its clinical use. Accumulating evidence shows that NM23-H1 has a dichotomous role in tumor metastasis as a suppressor and promoter. It has potentially attributed to its versatile biochemical characteristics such as nucleoside diphosphate kinase (NDPK) activity, histidine kinase activity (HPK), exonuclease activity, and protein scaffold, which further augment the complexity and uncertainty of its physiological function. Simultaneously, tumor cells have evolved multiple ways to regulate the expression and function of NM23-H1 during tumorigenesis and metastasis. This review summarized and discussed the regulatory mechanisms of NM23-H1 in cancer including transcriptional activation, subcellular location, enzymatic activity, and protein degradation, which significantly modulate its anti-metastatic function.

In this paper, we use spectroscopic methods (fluorescence spectroscopy, UV absorption spectroscopy, and circular dichroism (CD) spectroscopy) to elucidate the effects of reactive oxygen species generated by γ-irradiation on the molecular properties of human serum albumin (HSA). The results of fluorescence spectroscopy indicated that oxidation by γ-irradiation can lead to conformational changes of HSA. Data of CD spectra suggested that with the increase of radiation dose the percentage of α-helix in HSA has decreased. The determination of protein hydrophobicity showed that the effective hydrophobicity of HSA decreased up to 62% compared to the native HSA solution due to the exposure to the γ-irradiation. Furthermore, small changes in the esterase-like activity of HSA were introduced because of oxidation. The content of bityrosine increased markedly, suggesting that the oxidized HSA was aggregated. Moreover, there was no obvious change in the molecular properties of HSA with low γ-irradiation dose. Changes happened when the irradiation dose exceeded 200 Gy.

Polymeric nerve guidance conduits (NGCs) with uniform tubular structure are widely used as scaffolds in nerve tissue engineering. However, massive collapse of NGCs has greatly impeded their further application. Therefore, the gradient degradable nerve guidance conduit (GD-NGC) with multilayer structure is designed and fabricated via electrospinning technique. The GD-NGC consists of five poly(lactic-co-glycolic acid) (PLGA) layers with different polylactic acid (PLA)/polyglycolic acid (PGA) ratios. Compared to common NGCs, the novel GD-NGC degrades moderately and stepwise from inner to outer layers and also exhibits equivalent or better characteristics, such as porosity, water absorption capacity, mechanical property and biocompatibility. Collectively, GD-NGC has a promising potential for applications in nerve tissue engineering.

The clinical success of inhibitors targeting the PD-1/PD-L1 pathway has made this an active field in cancer immunotherapy. Currently, most drugs targeting this pathway are monoclonal antibodies. Small-molecule inhibitors as the alternative to monoclonal antibodies are expected to overcome the disadvantages of mAbs which include production difficulties and their long half-life. Recently, progress has been reported on anti-PD-1/PD-L1 small-molecule inhibitors. In this paper, we review the development of inhibitors targeting the PD-1/PD-L1 pathway, focusing mainly on peptide-based and nonpeptidic small-molecule inhibitors. The structures and the preclinical and clinical studies of several peptide-based small-molecule candidate compounds in clinical trials are discussed. We also illustrate the design strategies underlying reported nonpeptidic small-molecule inhibitors and provide insight into possible future exploration. Development of small-molecule drugs for anti-PD-1/PD-L1 activity with specific cancer applications is a promising and challenging prospect.

SET is a multifunctional oncoprotein which is ubiquitously expressed in all kinds of cells. The SET protein participates in many cellular processes including cell cycle, cell migration, apoptosis, transcription, and DNA repair. Accumulating evidence demonstrates that the expression and activity of SET correlate with cancer occurrence, metastasis, and prognosis. Therefore, the SET protein is regarded as a potential target for cancer therapy and several inhibitors are being developed for clinical use. Herein, we comprehensively review the physiological and pathological functions of SET as well as its structure‐function relationship. Additionally, the regulatory mechanisms of SET at both transcriptional and posttranslational levels are also discussed.

The cruciferous herb Weixian radish (Raphanus sativus L.), also known as Lai Fu, is a popular type of edible vegetable. The present paper describes the molecular tracking and bioactivity of glucocerebroside isolated from Weixian radish for the first time. Methanol extraction was carried out by using silica gel, Sephadex LH-20 and RP-C18 column chromatography. Based on their structures, the two compounds were determined to be 1-O-(β-D-glucopyranosyl)-(2S, 3S, 4R, 8E)-2-[(2'R)-2'-hydroxyl-tetracos-15'-enoyl amino]-8-octa-decene- 1, 3, 4-triol (glucocerebroside). The glucocerebroside could inhibit the growth of BEL-7402 cancer cells and induce apoptosis in these cells.

IntroductionSuccessful surgical treatment of congenital heart disease improves neonates’ long-term survival and leads to catch-up growth, which however does not occur in part of the patient population for largely undetermined reasons.Methods and analysisA multicentre, prospective cohort study is being conducted in four paediatric medical institutions in China to collect detailed nutritional, anthropometric and clinical data at perioperative phases and during a 1-year period of follow-up after surgery. The study is expected to recruit approximately 5000 patients by the year of 2023 when the cohort is fully established. The primary endpoint of this study is the occurrence of postoperative catch-up growth, which will be determined in both absolute and relative terms (ie, reduced anthropometric deficits from the reference measures and improved z-scores that have passed the −2 SD cut-offs). Multivariable regression analyses will be performed to identify factors that are statistically significantly associated with the absence of postoperative catch-up growth.Ethics and disseminationThe protocol of this study has been approved by the individual ethics committees of the participating centres (Guangzhou Women and Children’s Medical Centre (2008071601), the Children’s Hospital of Zhejiang University School of Medicine (2018-IRB-094), Gansu Provincial Maternity and Child-Care Hospital (2019-IRB-01) and Zhengzhou Cardiovascular Hospital (2019012001)). Written informed consent from parents will be obtained before study entry. Findings of this study will be disseminated through publications in international peer-reviewed journals and will be presented in academic conferences.

Objective The aim of our study was to introduce the surgical method and evaluate the efficacy of double sleeve lobectomy of the bronchus and the pulmonary artery in treatment for the central lung cancer.

In this paper, we use spectroscopic methods (fluorescence spectroscopy, UV absorption spectroscopy, and circular dichroism (CD) spectroscopy) to elucidate the effects of reactive oxygen species generated by γ-irradiation on the molecular properties of human serum albumin (HSA). The results of fluorescence spectroscopy indicated that oxidation by γ-irradiation can lead to conformational changes of HSA. Data of CD spectra suggested that with the increase of radiation dose the percentage of α-helix in HSA has decreased. The determination of protein hydrophobicity showed that the effective hydrophobicity of HSA decreased up to 62% compared to the native HSA solution due to the exposure to the γ-irradiation. Furthermore, small changes in the esterase-like activity of HSA were introduced because of oxidation. The content of bityrosine increased markedly, suggesting that the oxidized HSA was aggregated. Moreover, there was no obvious change in the molecular properties of HSA with low γ-irradiation dose. Changes happened when the irradiation dose exceeded 200 Gy.