Publications by authors named "Xiaoyong Fu"

52 Publications

Changes in physicochemical properties and microfauna community during vermicomposting of municipal sludge under different moisture conditions.

Environ Sci Pollut Res Int 2021 Feb 19. Epub 2021 Feb 19.

State Key Laboratory of Pollution Control and Source Reuse, Tongji University, Shanghai, 200092, China.

The present study aimed to explore the effect of a range of moisture content levels, including 65%, 72%, and 78%, on physicochemical properties and microfauna communities during vermicomposting of municipal sludge. As a result, death of perishable microfauna together with the degradation of organic matter was the dominant response in all groups in the early period of vermicomposting, while the effects of moisture content levels on various physiochemical parameters did not appear until the mid-later period. After the treatment with 78% moisture content, the content of mineral nitrogen was 1.186 g/kg in the sludge, with a 9.36 × 10 ind./g of microfauna quantity and 663.01 g of earthworm biomass. The values of these three measurements in 78% group were significantly higher than other two groups (p < 0.05), indicating that the effects of 78% moisture content were more pronounced for promoting nitrogen mineralization as well as microfauna and earthworms growth during vermicomposting. Specifically, testate amoebae were strongly associated with nitrification process, while nematodes were related to ammonification and phosphorus mineralization, of which testate amoebae had great potential of being bioindicators during vermicomposting of municipal sludge.
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http://dx.doi.org/10.1007/s11356-021-12846-5DOI Listing
February 2021

Activation of the IFN Signaling Pathway is Associated with Resistance to CDK4/6 Inhibitors and Immune Checkpoint Activation in ER-Positive Breast Cancer.

Clin Cancer Res 2021 Feb 3. Epub 2021 Feb 3.

Lester and Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas.

Purpose: Cyclin-dependent kinase 4 (CDK4) and CDK6 inhibitors (CDK4/6i) are highly effective against estrogen receptor-positive (ER)/HER2 breast cancer; however, intrinsic and acquired resistance is common. Elucidating the molecular features of sensitivity and resistance to CDK4/6i may lead to identification of predictive biomarkers and novel therapeutic targets, paving the way toward improving patient outcomes.

Experimental Design: Parental breast cancer cells and their endocrine-resistant derivatives (EndoR) were used. Derivatives with acquired resistance to palbociclib (PalboR) were generated from parental and estrogen deprivation-resistant MCF7 and T47D cells. Transcriptomic and proteomic analyses were performed in palbociclib-sensitive and PalboR lines. Gene expression data from CDK4/6i neoadjuvant trials and publicly available datasets were interrogated for correlations of gene signatures and patient outcomes.

Results: Parental and EndoR breast cancer lines showed varying degrees of sensitivity to palbociclib. Transcriptomic analysis of these cell lines identified an association between high IFN signaling and reduced CDK4/6i sensitivity; thus an "IFN-related palbociclib-resistance Signature" (IRPS) was derived. In two neoadjuvant trials of CDK4/6i plus endocrine therapy, IRPS and other IFN-related signatures were highly enriched in patients with tumors exhibiting intrinsic resistance to CDK4/6i. PalboR derivatives displayed dramatic activation of IFN/STAT1 signaling compared with their short-term treated or untreated counterparts. In primary ER/HER2 tumors, the IRPS score was significantly higher in lumB than lumA subtype and correlated with increased gene expression of immune checkpoints, endocrine resistance, and poor prognosis.

Conclusions: Aberrant IFN signaling is associated with intrinsic resistance to CDK4/6i. Experimentally, acquired resistance to palbociclib is associated with activation of the IFN pathway, warranting additional studies to clarify its involvement in resistance to CDK4/6i.
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http://dx.doi.org/10.1158/1078-0432.CCR-19-4191DOI Listing
February 2021

Enhancer reprogramming driven by high-order assemblies of transcription factors promotes phenotypic plasticity and breast cancer endocrine resistance.

Nat Cell Biol 2020 06 18;22(6):701-715. Epub 2020 May 18.

Department of Molecular Medicine, Mays Cancer Center, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.

Acquired therapy resistance is a major problem for anticancer treatment, yet the underlying molecular mechanisms remain unclear. Using an established breast cancer cellular model, we show that endocrine resistance is associated with enhanced phenotypic plasticity, indicated by a general downregulation of luminal/epithelial differentiation markers and upregulation of basal/mesenchymal invasive markers. Consistently, similar gene expression changes are found in clinical breast tumours and patient-derived xenograft samples that are resistant to endocrine therapies. Mechanistically, the differential interactions between oestrogen receptor α and other oncogenic transcription factors, exemplified by GATA3 and AP1, drive global enhancer gain/loss reprogramming, profoundly altering breast cancer transcriptional programs. Our functional studies in multiple culture and xenograft models reveal a coordinated role of GATA3 and AP1 in re-organizing enhancer landscapes and regulating cancer phenotypes. Collectively, our study suggests that differential high-order assemblies of transcription factors on enhancers trigger genome-wide enhancer reprogramming, resulting in transcriptional transitions that promote tumour phenotypic plasticity and therapy resistance.
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http://dx.doi.org/10.1038/s41556-020-0514-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7737911PMC
June 2020

Discovery, Structure-Activity Relationship, and Biological Activity of Histone-Competitive Inhibitors of Histone Acetyltransferases P300/CBP.

J Med Chem 2020 05 21;63(9):4716-4731. Epub 2020 Apr 21.

Avera Institute for Human Genetics, Sioux Falls, South Dakota 57108, United States.

Histone acetyltransferase (HAT) p300 and its paralog CBP acetylate histone lysine side chains and play critical roles in regulating gene transcription. The HAT domain of p300/CBP is a potential drug target for cancer. Through compound screening and medicinal chemistry, novel inhibitors of p300/CBP HAT with their IC values as low as 620 nM were discovered. The most potent inhibitor is competitive against histone substrates and exhibits a high selectivity for p300/CBP. It inhibited cellular acetylation and had strong activity with EC of 1-3 μM against proliferation of several tumor cell lines. Gene expression profiling in estrogen receptor (ER)-positive breast cancer MCF-7 cells showed that inhibitor treatment recapitulated siRNA-mediated p300 knockdown, inhibited ER-mediated gene transcription, and suppressed expression of numerous cancer-related gene signatures. These results demonstrate that the inhibitor is not only a useful probe for biological studies of p300/CBP HAT but also a pharmacological lead for further drug development targeting cancer.
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http://dx.doi.org/10.1021/acs.jmedchem.9b02164DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7340344PMC
May 2020

Author Correction: Temporal dynamic reorganization of 3D chromatin architecture in hormone-induced breast cancer and endocrine resistance.

Nat Commun 2020 04 20;11(1):1967. Epub 2020 Apr 20.

Department of Molecular Medicine, University of Texas Health San Antonio, San Antonio, TX, 78229, USA.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.
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http://dx.doi.org/10.1038/s41467-020-15789-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7170926PMC
April 2020

Estrogen-induced transcription at individual alleles is independent of receptor level and active conformation but can be modulated by coactivators activity.

Nucleic Acids Res 2020 02;48(4):1800-1810

Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.

Steroid hormones are pivotal modulators of pathophysiological processes in many organs, where they interact with nuclear receptors to regulate gene transcription. However, our understanding of hormone action at the single cell level remains incomplete. Here, we focused on estrogen stimulation of the well-characterized GREB1 and MYC target genes that revealed large differences in cell-by-cell responses, and, more interestingly, between alleles within the same cell, both over time and hormone concentration. We specifically analyzed the role of receptor level and activity state during allele-by-allele regulation and found that neither receptor level nor activation status are the determinant of maximal hormonal response, indicating that additional pathways are potentially in place to modulate cell- and allele-specific responses. Interestingly, we found that a small molecule inhibitor of the arginine methyltransferases CARM1 and PRMT6 was able to increase, in a gene specific manner, the number of active alleles/cell before and after hormonal stimulation, suggesting that mechanisms do indeed exist to modulate hormone receptor responses at the single cell and allele level.
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http://dx.doi.org/10.1093/nar/gkz1172DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7039002PMC
February 2020

FOXA1 upregulation promotes enhancer and transcriptional reprogramming in endocrine-resistant breast cancer.

Proc Natl Acad Sci U S A 2019 Dec 11. Epub 2019 Dec 11.

Lester and Sue Smith Breast Center, Baylor College of Medicine, Houston, TX 77030;

Forkhead box A1 (FOXA1) is a pioneer factor that facilitates chromatin binding and function of lineage-specific and oncogenic transcription factors. Hyperactive FOXA1 signaling due to gene amplification or overexpression has been reported in estrogen receptor-positive (ER) endocrine-resistant metastatic breast cancer. However, the molecular mechanisms by which FOXA1 up-regulation promotes these processes and the key downstream targets of the FOXA1 oncogenic network remain elusive. Here, we demonstrate that FOXA1 overexpression in ER breast cancer cells drives genome-wide enhancer reprogramming to activate prometastatic transcriptional programs. Up-regulated FOXA1 employs superenhancers (SEs) to synchronize transcriptional reprogramming in endocrine-resistant breast cancer cells, reflecting an early embryonic development process. We identify the hypoxia-inducible transcription factor hypoxia-inducible factor-2α (HIF-2α) as the top high FOXA1-induced SE target, mediating the impact of high FOXA1 in activating prometastatic gene sets and pathways associated with poor clinical outcome. Using clinical ER/HER2 metastatic breast cancer datasets, we show that the aberrant FOXA1/HIF-2α transcriptional axis is largely nonconcurrent with the mutations, suggesting different mechanisms of endocrine resistance and treatment strategies. We further demonstrate the selective efficacy of an HIF-2α antagonist, currently in clinical trials for advanced kidney cancer and recurrent glioblastoma, in reducing the clonogenicity, migration, and invasion of endocrine-resistant breast cancer cells expressing high FOXA1. Our study has uncovered high FOXA1-induced enhancer reprogramming and HIF-2α-dependent transcriptional programs as vulnerable targets for treating endocrine-resistant and metastatic breast cancer.
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http://dx.doi.org/10.1073/pnas.1911584116DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6936436PMC
December 2019

In vivo longitudinal imaging of RNA interference-induced endocrine therapy resistance in breast cancer.

J Biophotonics 2020 01 9;13(1):e201900180. Epub 2019 Oct 9.

Division of Molecular Imaging, Department of Radiology, Baylor College of Medicine, Houston, Texas.

Endocrine therapy resistance in breast cancer is a major obstacle in the treatment of patients with estrogen receptor-positive (ER+) tumors. Herein, we demonstrate the feasibility of longitudinal, noninvasive and semiquantitative in vivo molecular imaging of resistance to three endocrine therapies by using an inducible fluorescence-labeled short hairpin RNA (shRNA) system in orthotopic mice xenograft tumors. We employed a dual fluorescent doxycycline (Dox)-regulated lentiviral inducer system to transfect ER+ MCF7L breast cancer cells, with green fluorescent protein (GFP) expression as a marker of transfection and red fluorescent protein (RFP) expression as a surrogate marker of Dox-induced tumor suppressor phosphatase and tensin homolog deleted on chromosome 10 (PTEN) knockdown. Xenografted MCF7L tumor-bearing nude mice were randomized to therapies comprising estrogen deprivation, tamoxifen or an ER degrader (fulvestrant) and an estrogen-treated control group. Longitudinal imaging was performed by a home-built multispectral imaging system based on a cooled image intensified charge coupled device camera. The GFP signal, which corresponds to number of viable tumor cells, exhibited excellent correlation to caliper-measured tumor size (P < .05). RFP expression was substantially higher in mice exhibiting therapy resistance and strongly and significantly (P < 1e-7) correlated with the tumor size progression for the mice with shRNA-induced PTEN knockdown. PTEN loss was strongly correlated with resistance to estrogen deprivation, tamoxifen and fulvestrant therapies.
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http://dx.doi.org/10.1002/jbio.201900180DOI Listing
January 2020

Targeting the Mevalonate Pathway to Overcome Acquired Anti-HER2 Treatment Resistance in Breast Cancer.

Mol Cancer Res 2019 11 16;17(11):2318-2330. Epub 2019 Aug 16.

Lester & Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas.

Despite effective strategies, resistance in HER2 breast cancer remains a challenge. While the mevalonate pathway (MVA) is suggested to promote cell growth and survival, including in HER2 models, its potential role in resistance to HER2-targeted therapy is unknown. Parental HER2 breast cancer cells and their lapatinib-resistant and lapatinib + trastuzumab-resistant derivatives were used for this study. MVA activity was found to be increased in lapatinib-resistant and lapatinib + trastuzumab-resistant cells. Specific blockade of this pathway with lipophilic but not hydrophilic statins and with the N-bisphosphonate zoledronic acid led to apoptosis and substantial growth inhibition of R cells. Inhibition was rescued by mevalonate or the intermediate metabolites farnesyl pyrophosphate or geranylgeranyl pyrophosphate, but not cholesterol. Activated Yes-associated protein (YAP)/transcriptional coactivator with PDZ-binding motif (TAZ) and mTORC1 signaling, and their downstream target gene product Survivin, were inhibited by MVA blockade, especially in the lapatinib-resistant/lapatinib + trastuzumab-resistant models. Overexpression of constitutively active YAP rescued Survivin and phosphorylated-S6 levels, despite blockade of the MVA. These results suggest that the MVA provides alternative signaling leading to cell survival and resistance by activating YAP/TAZ-mTORC1-Survivin signaling when HER2 is blocked, suggesting novel therapeutic targets. MVA inhibitors including lipophilic statins and N-bisphosphonates may circumvent resistance to anti-HER2 therapy warranting further clinical investigation. IMPLICATIONS: The MVA was found to constitute an escape mechanism of survival and growth in HER2 breast cancer models resistant to anti-HER2 therapies. MVA inhibitors such as simvastatin and zoledronic acid are potential therapeutic agents to resensitize the tumors that depend on the MVA to progress on anti-HER2 therapies.
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http://dx.doi.org/10.1158/1541-7786.MCR-19-0756DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6825570PMC
November 2019

Gut digestion of earthworms significantly attenuates cell-free and -associated antibiotic resistance genes in excess activated sludge by affecting bacterial profiles.

Sci Total Environ 2019 Nov 12;691:644-653. Epub 2019 Jul 12.

River Basin Research Center, Gifu University, 1-1 Yanagido, Gifu 501-1193, Japan; School of Environment and Energy, South China University of Technology, Guangzhou 510006, China. Electronic address:

Vermicomposting can significantly attenuate antibiotic resistance genes (ARGs) in the excess activated sludge (EAS). However, the effect of earthworms, especially the effect of gut digestion as a critical step in the vermicomposting process, remains unclarified. The purpose of this study was to investigate the response of ARGs (cell-free and -associated) in EAS to gut digestion of earthworms and to clarify the possible mechanism from the viewpoint of bacterial community through quantitative polymer chain reaction (q-PCR) and high throughput sequencing. Compared to the initial sludge, the earthworm casts were observed to have significantly lower absolute abundances of ARGs, especially qnrS, tetM, and tetX with the removal exceeding 90%. Cell-free and -associated ARGs (except sul1 and tetG) had equivalent contributions to the attenuation of each ARG. Remarkable reductions of bacterial number and alpha diversity (chao1 and Shannon) were detected in the casts. Spearman correlation analysis between the targeted genes and bacterial community indicates that twelve different phyla mainly including Acidobacteria, Euryarchaeota, Deinococcus-Thermus, Chlorobi, Firmicutes, Fibrobacteres, and Proteobacteria are the potential ARGs hosts, suggesting that the fate and behaviour of these hosts during gut digestion of EAS by earthworms substantially determined the dynamics of the ARGs. These findings increase our understanding of earthworm gut digestion as an important process for the attenuation of ARGs in EAS, and contribute towards preventing their release into the total environment.
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http://dx.doi.org/10.1016/j.scitotenv.2019.07.177DOI Listing
November 2019

Integrated RFA/PSOCT catheter for real-time guidance of cardiac radio-frequency ablation.

Biomed Opt Express 2018 Dec 20;9(12):6400-6411. Epub 2018 Nov 20.

Department of Biomedical Engineering, Case Western Reserve University, Cleveland, OH 44106, USA.

Radiofrequency ablation (RFA) is an important standard therapy for cardiac arrhythmias, but direct monitoring of tissue treatment is currently lacking. We demonstrate an RFA catheter integrated with polarization sensitive optical coherence tomography (PSOCT) for directly monitoring the RFA process in real time. The integrated RFA/OCT catheter was modified from a standard clinical RFA catheter and includes a miniature forward-viewing cone-scanning OCT probe. The PSOCT system was validated with a quarter-wave plate while the RFA function of the integrated catheter was validated by comparing lesion sizes with those made with an unmodified RFA catheter. Additionally, the integrated catheter guided catheter-tissue apposition and monitored RFA lesion formation in cardiac tissue in real time. The results show that catheter-tissue contact can be characterized by observing the features of the blood and tissue in the acquired OCT images and that RFA lesion formation can be confirmed by monitoring the change in phase retardance in the acquired PSOCT images. This system demonstrates the feasibility of an integrated RFA/OCT catheter to deliver RF energy and image the cardiac wall simultaneously and justifies further research into use of this technology to aid RFA therapy for cardiac arrhythmias.
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http://dx.doi.org/10.1364/BOE.9.006400DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6490984PMC
December 2018

Temporal dynamic reorganization of 3D chromatin architecture in hormone-induced breast cancer and endocrine resistance.

Nat Commun 2019 04 3;10(1):1522. Epub 2019 Apr 3.

Department of Molecular Medicine, University of Texas Health San Antonio, San Antonio, TX, 78229, USA.

Recent studies have demonstrated that chromatin architecture is linked to the progression of cancers. However, the roles of 3D structure and its dynamics in hormone-dependent breast cancer and endocrine resistance are largely unknown. Here we report the dynamics of 3D chromatin structure across a time course of estradiol (E2) stimulation in human estrogen receptor α (ERα)-positive breast cancer cells. We identified subsets of temporally highly dynamic compartments predominantly associated with active open chromatin and found that these highly dynamic compartments showed higher alteration in tamoxifen-resistant breast cancer cells. Remarkably, these compartments are characterized by active chromatin states, and enhanced ERα binding but decreased transcription factor CCCTC-binding factor (CTCF) binding. We finally identified a set of ERα-bound promoter-enhancer looping genes enclosed within altered domains that are enriched with cancer invasion, aggressiveness or metabolism signaling pathways. This large-scale analysis expands our understanding of high-order temporal chromatin reorganization underlying hormone-dependent breast cancer.
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http://dx.doi.org/10.1038/s41467-019-09320-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6447566PMC
April 2019

Implications of Classification of Os Trigonum: A Study Based on Computed Tomography Three-Dimensional Imaging.

Med Sci Monit 2019 Feb 22;25:1423-1428. Epub 2019 Feb 22.

Department of Orthopedic, Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou, Sichuan, China (mainland).

BACKGROUND The os trigonum is an accessory bone that is not fully fused with the talus during secondary ossification, and is one of the risk factors of posterior malleolus impact syndrome. The purpose of this study was to classify the os trigonum and to guide the diagnosis and treatment of related clinical diseases. MATERIAL AND METHODS Ankle computed tomography (CT) scans of 586 Chinese patients between October 2014 and October 2018 were reviewed. CT images of 1011 ankle joints were reconstructed to evaluate the classification of the os trigonum and the measurement of anatomical parameters. RESULTS The incidences of os trigonum in 3 groups were determined as type I (1.9%), type II (10.5%), and type III (14.7%). The macro-axis of type II (0.89±0.31) cm was significantly larger than with type I (0.65±0.24 cm) and type III (0.74±0.23 cm) (p<0.05).The minor axis of similar of type I (0.41±0.23 cm) was significantly shorter than that of type II (0.58±0.32 cm) and type III (0.55±0.16 cm) (p<0.05).The distance from os trigonum to calcaneal tubercle was significantly different than that of type I (1.33±0.52 cm), type II (1.67±0.55 cm), and type III (1.84±0.45 cm) (p<0.05). CONCLUSIONS This study showed that os trigonum has a high incidence. Type I was the least common, the volume of type II was larger, and type III was more common. The anatomical parameters of each type may improve treatment of related diseases and the further development of ankle arthroscopic surgery.
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http://dx.doi.org/10.12659/MSM.914485DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6396439PMC
February 2019

The oral selective oestrogen receptor degrader (SERD) AZD9496 is comparable to fulvestrant in antagonising ER and circumventing endocrine resistance.

Br J Cancer 2019 02 17;120(3):331-339. Epub 2018 Dec 17.

Lester & Sue Smith Breast Center, Baylor College of Medicine, Houston, TX, 77030, USA.

Background: The oestrogen receptor (ER) is an important therapeutic target in ER-positive (ER+) breast cancer. The selective ER degrader (SERD), fulvestrant, is effective in patients with metastatic breast cancer, but its intramuscular route of administration and low bioavailability are major clinical limitations.

Methods: Here, we studied the pharmacology of a new oral SERD, AZD9496, in a panel of in vitro and in vivo endocrine-sensitive and -resistant breast cancer models.

Results: In endocrine-sensitive models, AZD9496 inhibited cell growth and blocked ER activity in the presence or absence of oestrogen. In vivo, in the presence of oestrogen, short-term AZD9496 treatment, like fulvestrant, resulted in tumour growth inhibition and reduced expression of ER-dependent genes. AZD9496 inhibited cell growth in oestrogen deprivation-resistant and tamoxifen-resistant cell lines and xenograft models that retain ER expression. AZD9496 effectively reduced ER levels and ER-induced transcription. Expression analysis of short-term treated tumours showed that AZD9496 potently inhibited classic oestrogen-induced gene transcription, while simultaneously increasing expression of genes negatively regulated by ER, including genes potentially involved in escape pathways of endocrine resistance.

Conclusions: These data suggest that AZD9496 is a potent anti-oestrogen that antagonises and degrades ER with anti-tumour activity in both endocrine-sensitive and endocrine-resistant models.
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http://dx.doi.org/10.1038/s41416-018-0354-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6353941PMC
February 2019

Nitrogen removal of anaerobically digested swine wastewater by pilot-scale tidal flow constructed wetland based on in-situ biological regeneration of zeolite.

Chemosphere 2019 Feb 5;217:364-373. Epub 2018 Nov 5.

College of Environmental Science and Engineering, Hunan University and Key Laboratory of Environmental Biology and Pollution Control (Hunan University), Ministry of Education, Changsha, Hunan 410082, China.

Dispersed swine wastewater has increasingly aggravated water pollution in China. Anaerobically digested dispersed swine wastewater was targeted and treated by a pilot-scale zoning tidal flow constructed wetland (TFCW) with a bottom wastewater saturation layer. The long-term application of in-situ biological regeneration of biozeolite, nitrogen removal performance, nitrogen removal pathways and microbial community of TFCW were investigated. Results showed that with the surface loads of 0.079, 0.022 and 0.024 kg/(m·d), TFCW could decrease COD, NHN and TN by 84.75%, 74.13% and 67.13% respectively. Influent COD, NHN, TN and nitrates/nitrites produced by bioregeneration of NHN were mostly removed in zeolite layer and the remaining nitrates/nitrites could be further denitrified in bottom saturation layer. Theory of dynamic process of rapid-adsorption and bioregeneration for NHN removal was proposed. When this process reached dynamic equilibrium, the mass of adsorbed NHN onto zeolites remained relatively stable. When ambient temperature decreased to 16 °C, TFCW could still remove COD, NHN and TN by 73.79%, 72.99% and 70.71% with the surface loads of 0.103, 0.056 and 0.054 kg/(m·d) respectively. Nitrification-denitrification which accounted for 80.32% of TN removal was the main nitrogen removal pathway. Dominant nitrifiers (Nitrosospira and Rhizomicrobium) and denitrifiers (Ottowia, Thauera and Rhodanobacteria) in biozeolite layer verified the existence of simultaneous nitrification and denitrification.
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http://dx.doi.org/10.1016/j.chemosphere.2018.11.036DOI Listing
February 2019

Changes of quinolone resistance genes and their relations with microbial profiles during vermicomposting of municipal excess sludge.

Sci Total Environ 2018 Dec 11;644:494-502. Epub 2018 Jul 11.

School of Environmental and Municipal Engineering, Lanzhou Jiaotong University, Lanzhou 730070, China.

Antibiotic resistance genes abundant in municipal excess sludge reduce the agricultural value of vermicompost. However, little attention has been paid on the fate and behavior of the problem-causing agents in vermicomposting. In this study, the fate and behavior of quinolone resistance genes in excess activated sludge during vermicomposting were studied with reactors introduced with Eisenia fetida for three different densities. The substrate pile without earthworms was operated as control in parallel. The results showed that earthworms could significantly reduce the absolute abundance of quinolone resistance genes in the excess sludge, with a reduction ratio of 85.6-100% for qnr A and 92.3-95.3% for qnr S, respectively (p < 0.05). For microbial profiles, both the dehydrogenase activity and the abundance of microbes (16S rDNA) revealed a distinct decreasing trend after 7 days from the start of the experiment; however, the bacterial diversity in the final products seemed to be enriched with the emergence of the uncultured Flavobacteriales bacterium and uncultured Anaerolineaceae bacterium. Redundancy analysis revealed clearly that the qnr genes had positive correlations with the targeted indexes of microbial profiles, with the correlations with the bacterial abundance and dehydrogenase activity being more statistically significant than the bacterial diversity (p < 0.05). The results of this study suggested that earthworms could promote the attenuation of quinolone resistance genes in the excess sludge through lowering the bacterial abundance and activity, and the promotion effect could be enhanced by increasing the density of earthworms.
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http://dx.doi.org/10.1016/j.scitotenv.2018.07.015DOI Listing
December 2018

GPCRs profiling and identification of GPR110 as a potential new target in HER2+ breast cancer.

Breast Cancer Res Treat 2018 Jul 24;170(2):279-292. Epub 2018 Mar 24.

Department of Pharmacy Practice and Translational Research, University of Houston, 4849 Calhoun St, Houston, TX, 77204, USA.

Purpose: G protein-coupled receptors (GPCRs) represent the largest family of druggable targets in human genome. Although several GPCRs can cross-talk with the human epidermal growth factor receptors (HERs), the expression and function of most GPCRs remain unknown in HER2+ breast cancer (BC). In this study, we aimed to evaluate gene expression of GPCRs in tumorigenic or anti-HER2 drug-resistant cells and to understand the potential role of candidate GPCRs in HER2+ BC.

Methods: Gene expression of 352 GPCRs was profiled in Aldeflur+ tumorigenic versus Aldeflur- population and anti-HER2 therapy-resistant derivatives versus parental cells of HER2+ BT474 cells. The GPCR candidates were confirmed in 7 additional HER2+ BC cell line models and publicly available patient dataset. Anchorage-dependent and anchorage-independent cell growth, mammosphere formation, and migration/invasion were evaluated upon GPR110 knockdown by siRNA in BT474 and SKBR3 parental and lapatinib+ trastuzumab-resistant (LTR) cells.

Results: Adhesion and class A GPCRs were overexpressed in Aldeflur+ and anti-HER2 therapy-resistant population of BT474 cells, respectively. GPR110 was the only GPCR overexpressed in Aldeflur+ and anti-HER2 therapy-resistant population in BT474, SKBR3, HCC1569, MDA-MB-361, AU565, and/or HCC202 cells and in HER2+ BC subtype in patient tumors. Using BT474 and SKBR3 parental and LTR cells, we found that GPR110 knockdown significantly reduced anchorage-dependent/independent cell growth as well as migration/invasion of parental and LTR cells and mammosphere formation in LTR derivatives and not in parental cells.

Conclusion: Our data suggest a potential role of GPR110 in tumorigenicity and in tumor cell dissemination in HER2+ BC.
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http://dx.doi.org/10.1007/s10549-018-4751-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6110614PMC
July 2018

Tamoxifen Resistance in Breast Cancer Is Regulated by the EZH2-ERα-GREB1 Transcriptional Axis.

Cancer Res 2018 02 6;78(3):671-684. Epub 2017 Dec 6.

Department of Molecular Medicine, University of Texas Health Science Center, San Antonio, Texas.

Resistance to cancer treatment can be driven by epigenetic reprogramming of specific transcriptomes in favor of the refractory phenotypes. Here we discover that tamoxifen resistance in breast cancer is driven by a regulatory axis consisting of a master transcription factor, its cofactor, and an epigenetic regulator. The oncogenic histone methyltransferase EZH2 conferred tamoxifen resistance by silencing the expression of the estrogen receptor α (ERα) cofactor GREB1. In clinical specimens, induction of DNA methylation of a particular CpG-enriched region at the promoter negatively correlated with levels and cell sensitivity to endocrine agents. GREB1 also ensured proper cellular reactions to different ligands by recruiting distinct sets of ERα cofactors to -regulatory elements, which explains the contradictory biological effects of GREB1 on breast cancer cell growth in response to estrogen or antiestrogen. In refractory cells, EZH2-dependent repression of GREB1 triggered chromatin reallocation of ERα coregulators, converting the antiestrogen into an agonist. In clinical specimens from patients receiving adjuvant tamoxifen treatment, expression levels of EZH2 and GREB1 were correlated negatively, and taken together better predicted patient responses to endocrine therapy. Overall, our work suggests a new strategy to overcome endocrine resistance in metastatic breast cancer by targeting a particular epigenetic program. This study suggests a new strategy to overcome endocrine resistance in metastatic breast cancer by targeting a particular epigenetic program defined within. .
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http://dx.doi.org/10.1158/0008-5472.CAN-17-1327DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5967248PMC
February 2018

Integrated molecular analysis of Tamoxifen-resistant invasive lobular breast cancer cells identifies MAPK and GRM/mGluR signaling as therapeutic vulnerabilities.

Mol Cell Endocrinol 2018 08 19;471:105-117. Epub 2017 Sep 19.

Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA. Electronic address:

Invasive lobular breast cancer (ILC) is an understudied malignancy with distinct clinical, pathological, and molecular features that distinguish it from the more common invasive ductal carcinoma (IDC). Mounting evidence suggests that estrogen receptor-alpha positive (ER+) ILC has a poor response to Tamoxifen (TAM), but the mechanistic drivers of this are undefined. In the current work, we comprehensively characterize the SUM44/LCCTam ILC cell model system through integrated analysis of gene expression, copy number, and mutation, with the goal of identifying actionable alterations relevant to clinical ILC that can be co-targeted along with ER to improve treatment outcomes. We show that TAM has several distinct effects on the transcriptome of LCCTam cells, that this resistant cell model has acquired copy number alterations and mutations that impinge on MAPK and metabotropic glutamate receptor (GRM/mGluR) signaling networks, and that pharmacological inhibition of either improves or restores the growth-inhibitory actions of endocrine therapy.
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http://dx.doi.org/10.1016/j.mce.2017.09.024DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5858970PMC
August 2018

Embryonic transcription factor SOX9 drives breast cancer endocrine resistance.

Proc Natl Acad Sci U S A 2017 05 15;114(22):E4482-E4491. Epub 2017 May 15.

Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02215;

The estrogen receptor (ER) drives the growth of most luminal breast cancers and is the primary target of endocrine therapy. Although ER blockade with drugs such as tamoxifen is very effective, a major clinical limitation is the development of endocrine resistance especially in the setting of metastatic disease. Preclinical and clinical observations suggest that even following the development of endocrine resistance, ER signaling continues to exert a pivotal role in tumor progression in the majority of cases. Through the analysis of the ER cistrome in tamoxifen-resistant breast cancer cells, we have uncovered a role for an RUNX2-ER complex that stimulates the transcription of a set of genes, including most notably the stem cell factor SOX9, that promote proliferation and a metastatic phenotype. We show that up-regulation of SOX9 is sufficient to cause relative endocrine resistance. The gain of SOX9 as an ER-regulated gene associated with tamoxifen resistance was validated in a unique set of clinical samples supporting the need for the development of improved ER antagonists.
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http://dx.doi.org/10.1073/pnas.1620993114DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5465894PMC
May 2017

FOXA1 overexpression mediates endocrine resistance by altering the ER transcriptome and IL-8 expression in ER-positive breast cancer.

Proc Natl Acad Sci U S A 2016 10 6;113(43):E6600-E6609. Epub 2016 Oct 6.

Lester and Sue Smith Breast Center, Baylor College of Medicine, Houston, TX 77030; Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030; Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030; Department of Medicine, Baylor College of Medicine, Houston, TX 77030;

Forkhead box protein A1 (FOXA1) is a pioneer factor of estrogen receptor α (ER)-chromatin binding and function, yet its aberration in endocrine-resistant (Endo-R) breast cancer is unknown. Here, we report preclinical evidence for a role of FOXA1 in Endo-R breast cancer as well as evidence for its clinical significance. FOXA1 is gene-amplified and/or overexpressed in Endo-R derivatives of several breast cancer cell line models. Induced FOXA1 triggers oncogenic gene signatures and proteomic profiles highly associated with endocrine resistance. Integrated omics data reveal IL8 as one of the most perturbed genes regulated by FOXA1 and ER transcriptional reprogramming in Endo-R cells. IL-8 knockdown inhibits tamoxifen-resistant cell growth and invasion and partially attenuates the effect of overexpressed FOXA1. Our study highlights a role of FOXA1 via IL-8 signaling as a potential therapeutic target in FOXA1-overexpressing ER-positive tumors.
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http://dx.doi.org/10.1073/pnas.1612835113DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5087040PMC
October 2016

Optimal growth condition of earthworms and their vermicompost features during recycling of five different fresh fruit and vegetable wastes.

Environ Sci Pollut Res Int 2016 Jul 17;23(13):13569-75. Epub 2016 May 17.

School of Environmental and Municipal Engineering, Lanzhou Jiaotong University, Lanzhou, 730070, China.

This study aimed to promote vermicomposting performance for recycling fresh fruit and vegetable wastes (FVWs) and to assess microbial population and community of final products. Five fresh FVWs including banana peels, cabbage, lettuce, potato, and watermelon peels were chosen as earthworms' food. The fate test of earthworms showed that 30 g fresh FVWs/day was the optimal loading and the banana peels was harmful for the survival of Eisenia fetida. The followed vermicomposting test revealed lower contents of total carbon and weaker microbial activity in final vermicomposts, relative to those in compared systems without earthworms worked. The leachate from FVWs carried away great amounts of nutrients from reactors. Additionally, different fresh FVWs displayed dissimilar stabilization process. Molecular biological approaches revealed that earthworms could broaden bacterial diversity in their products, with significant greater populations of actinobacteria and ammonia oxidizing bacteria than in control. This study evidences that vermicomposting efficiency differs with the types and loadings of fresh FVWs and vermicomposts are rich in agricultural probiotics.
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http://dx.doi.org/10.1007/s11356-016-6848-1DOI Listing
July 2016

Blockade of AP-1 Potentiates Endocrine Therapy and Overcomes Resistance.

Mol Cancer Res 2016 05 10;14(5):470-81. Epub 2016 Mar 10.

Lester and Sue Smith Breast Center and Dan L. Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, Texas. Department of Medicine, Baylor College of Medicine, Houston, Texas. Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas.

Unlabelled: The transcription factor AP-1 is downstream of growth factor (GF) receptors (GFRs) and stress-related kinases, both of which are implicated in breast cancer endocrine resistance. Previously, we have suggested that acquired endocrine resistance is associated with increased activity of AP-1 in an in vivo model. In this report, we provide direct evidence for the role of AP-1 in endocrine resistance. First, significant overlap was found between genes modulated in tamoxifen resistance and a gene signature associated with GF-induced estrogen receptor (ER) cistrome. Interestingly, these overlapping genes were enriched for key signaling components of GFRs and stress-related kinases and had AP-1 motifs in their promoters/enhancers. Second, to determine a more definitive role of AP-1 in endocrine resistance, AP-1 was inhibited using an inducible dominant-negative (DN) cJun expressed in MCF7 breast cancer cells in vitro and in vivo AP-1 blockade enhanced the antiproliferative effect of endocrine treatments in vitro, accelerated xenograft tumor response to tamoxifen and estrogen deprivation in vivo, promoted complete regression of tumors, and delayed the onset of tamoxifen resistance. Induction of DN-cJun after the development of tamoxifen resistance resulted in dramatic tumor shrinkage, accompanied by reduced proliferation and increased apoptosis. These data suggest that AP-1 is a key determinant of endocrine resistance by mediating a global shift in the ER transcriptional program.

Implications: AP-1 represents a viable therapeutic target to overcome endocrine resistance. Mol Cancer Res; 14(5); 470-81. ©2016 AACR.
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http://dx.doi.org/10.1158/1541-7786.MCR-15-0423DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4867274PMC
May 2016

Earthworms facilitate the stabilization of pelletized dewatered sludge through shaping microbial biomass and activity and community.

Environ Sci Pollut Res Int 2016 Mar 29;23(5):4522-30. Epub 2015 Oct 29.

School of Environmental and Municipal Engineering, Lanzhou Jiaotong University, Lanzhou, 730070, China.

In this study, the effect of earthworms on microbial features during vermicomposting of pelletized dewatered sludge (PDS) was investigated through comparing two degradation systems with and without earthworm E isenia fetida involvement. After 60 days of experimentation, a relatively stable product with low organic matter and high nitrate and phosphorous was harvested when the earthworms were involved. During the process, earthworms could enhance microbial activity and biomass at the initial stage and thus accelerating the rapid decomposition of PDS. The end products of vermicomposting allowed the lower values of bacterial and eukaryotic densities comparison with those of no earthworm addition. In addition, the presence of earthworms modified the bacterial and fungal diversity, making the disappearances of some pathogens and specific decomposing bacteria of recalcitrant substrates in the vermicomposting process. This study evidences that earthworms can facilitate the stabilization of PDS through modifying microbial activity and number and community during vermicomposting.
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http://dx.doi.org/10.1007/s11356-015-5659-0DOI Listing
March 2016

Upregulation of ER Signaling as an Adaptive Mechanism of Cell Survival in HER2-Positive Breast Tumors Treated with Anti-HER2 Therapy.

Clin Cancer Res 2015 Sep 26;21(17):3995-4003. Epub 2015 May 26.

Lester and Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas. Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas. Department of Medicine, Baylor College of Medicine, Houston, Texas.

Purpose: To investigate the direct effect and therapeutic consequences of epidermal growth factor receptor 2 (HER2)-targeting therapy on expression of estrogen receptor (ER) and Bcl2 in preclinical models and clinical tumor samples.

Experimental Design: Archived xenograft tumors from two preclinical models (UACC812 and MCF7/HER2-18) treated with ER and HER2-targeting therapies and also HER2+ clinical breast cancer specimens collected in a lapatinib neoadjuvant trial (baseline and week 2 posttreatment) were used. Expression levels of ER and Bcl2 were evaluated by immunohistochemistry and Western blot analysis. The effects of Bcl2 and ER inhibition, by ABT-737 and fulvestrant, respectively, were tested in parental versus lapatinib-resistant UACC812 cells in vitro.

Results: Expression of ER and Bcl2 was significantly increased in xenograft tumors with acquired resistance to anti-HER2 therapy compared with untreated tumors in both preclinical models (UACC812: ER P = 0.0014; Bcl2 P < 0.001 and MCF7/HER2-18: ER P = 0.0007; Bcl2 P = 0.0306). In the neoadjuvant clinical study, lapatinib treatment for 2 weeks was associated with parallel upregulation of ER and Bcl2 (Spearman coefficient: 0.70; P = 0.0002). Importantly, 18% of tumors originally ER-negative (ER(-)) converted to ER(+) upon anti-HER2 therapy. In ER(-)/HER2(+) MCF7/HER2-18 xenografts, ER reexpression was primarily observed in tumors responding to potent combination of anti-HER2 drugs. Estrogen deprivation added to this anti-HER2 regimen significantly delayed tumor progression (P = 0.018). In the UACC812 cells, fulvestrant, but not ABT-737, was able to completely inhibit anti-HER2-resistant growth (P < 0.0001).

Conclusions: HER2 inhibition can enhance or restore ER expression with parallel Bcl2 upregulation, representing an ER-dependent survival mechanism potentially leading to anti-HER2 resistance.
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http://dx.doi.org/10.1158/1078-0432.CCR-14-2728DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4558260PMC
September 2015

Miniature forward-viewing common-path OCT probe for imaging the renal pelvis.

Biomed Opt Express 2015 Apr 6;6(4):1164-71. Epub 2015 Mar 6.

Department of Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio 44106 USA.

We demonstrate an ultrathin flexible cone-scanning forward-viewing OCT probe which can fit through the working channel of a flexible ureteroscope for renal pelvis imaging. The probe is fabricated by splicing a 200 µm section of core-less fiber and a 150 µm section of gradient-index (GRIN) fiber to the end of a single mode (SM) fiber. The probe is designed for common-path OCT imaging where the back-reflection of the GRIN fiber/air interface is used as the reference signal. Optimum sensitivity was achieved with a 2 degree polished probe tip. A correlation algorithm was used to correct image distortion caused by non-uniform rotation of the probe. The probe is demonstrated by imaging human skin in vivo and porcine renal pelvis ex vivo and is suitable for imaging the renal pelvis in vivo for cancer staging.
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http://dx.doi.org/10.1364/BOE.6.001164DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4399657PMC
April 2015

Feasibility of vermistabilization for fresh pelletized dewatered sludge with earthworms Bimastus parvus.

Bioresour Technol 2015 Jan 8;175:646-50. Epub 2014 Nov 8.

School of Environmental and Municipal Engineering, Lanzhou Jiaotong University, Lanzhou 730070, China.

The aim of this study was to investigate the feasibility of vermistabilization of fresh pelletized dewatered sludges (PDS) without any bulking materials using earthworms Bimastus parvus. For this, two pelletized treatments with 4.5mm and 14.5mm fresh PDS and one without pelletized treatment were setup. Earthworm's fate test showed that earthworms could not survive in the treatment without pelletisation. For two pelletized treatments, B. parvus had a good life, producing great numbers of cocoons and hatchlings, after 60days. Vermicomposting of PDS resulted in the decreases of DOC, ammonia-nitrogen and microbial biomass and activity while increases of electrical conductivity and nitrate-nitrogen and available phosphorous. These findings suggest the stable and beneficial vermicomposts were achieved. The overall results evidenced that the fresh PDS without blending could be directly stabilized by vermicomposting and the vermireactor containing 4.5mm PDS displayed a better performance than 14.5mm PDS.
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http://dx.doi.org/10.1016/j.biortech.2014.11.007DOI Listing
January 2015

Overcoming endocrine resistance due to reduced PTEN levels in estrogen receptor-positive breast cancer by co-targeting mammalian target of rapamycin, protein kinase B, or mitogen-activated protein kinase kinase.

Breast Cancer Res 2014 Sep 11;16(5):430. Epub 2014 Sep 11.

Introduction: Activation of the phosphatidylinositol 3-kinase (PI3K) pathway in estrogen receptor α (ER)-positive breast cancer is associated with reduced ER expression and activity, luminal B subtype, and poor outcome. Phosphatase and tensin homolog (PTEN), a negative regulator of this pathway, is typically lost in ER-negative breast cancer. We set out to clarify the role of reduced PTEN levels in endocrine resistance, and to explore the combination of newly developed PI3K downstream kinase inhibitors to overcome this resistance.

Methods: Altered cellular signaling, gene expression, and endocrine sensitivity were determined in inducible PTEN-knockdown ER-positive/human epidermal growth factor receptor 2 (HER2)-negative breast cancer cell and/or xenograft models. Single or two-agent combinations of kinase inhibitors were examined to improve endocrine therapy.

Results: Moderate PTEN reduction was sufficient to enhance PI3K signaling, generate a gene signature associated with the luminal B subtype of breast cancer, and cause endocrine resistance in vitro and in vivo. The mammalian target of rapamycin (mTOR), protein kinase B (AKT), or mitogen-activated protein kinase kinase (MEK) inhibitors, alone or in combination, improved endocrine therapy, but the efficacy varied by PTEN levels, type of endocrine therapy, and the specific inhibitor(s). A single-agent AKT inhibitor combined with fulvestrant conferred superior efficacy in overcoming resistance, inducing apoptosis and tumor regression.

Conclusions: Moderate reduction in PTEN, without complete loss, can activate the PI3K pathway to cause endocrine resistance in ER-positive breast cancer, which can be overcome by combining endocrine therapy with inhibitors of the PI3K pathway. Our data suggests that the ER degrader fulvestrant, to block both ligand-dependent and -independent ER signaling, combined with an AKT inhibitor is an effective strategy to test in patients.
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http://dx.doi.org/10.1186/s13058-014-0430-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4303114PMC
September 2014

Fiber-optic catheter-based polarization-sensitive OCT for radio-frequency ablation monitoring.

Opt Lett 2014 Sep;39(17):5066-9

An all-fiber optic catheter-based polarization-sensitive optical coherence tomography system is demonstrated. A novel multiplexing method was used to illuminate the sample, splitting the light from a 58.5 kHz Fourier-domain mode-locked laser such that two different polarization states, alternated in time, are generated by two semiconductor optical amplifiers. A 2.3 mm forward-view cone-scanning catheter probe was designed, fabricated, and used to acquire sample scattering intensity and phase retardation images. The system was first verified with a quarter-wave plate and then by obtaining intensity and phase retardation images of high-birefringence plastic, human skin in vivo, and untreated and thermally ablated porcine myocardium ex vivo. The system can potentially in vivo image of the cardiac wall to aid radio-frequency ablation therapy for cardiac arrhythmias.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4424424PMC
http://dx.doi.org/10.1364/OL.39.005066DOI Listing
September 2014

Effects of earthworms on physicochemical properties and microbial profiles during vermicomposting of fresh fruit and vegetable wastes.

Bioresour Technol 2014 Oct 28;170:45-52. Epub 2014 Jul 28.

School of Environmental and Municipal Engineering, Lanzhou Jiaotong University, Lanzhou 730070, China.

This study aimed to investigate the effect of earthworms on physicochemical and microbial properties during vermicomposting of fresh fruit and vegetable wastes (FVW) by contrasting two decomposing systems of FVW with and without earthworms for 5weeks. Compared to control treatment (without earthworms), vermicomposting treatment resulted in a rapid decrease of electrical conductivity and losses of total carbon and nitrogen from the 2nd week. Quantitative PCR displayed that earthworms markedly enhanced bacterial and fungal densities, showing the higher values than control, during the whole decomposition process. In addition, denaturing gradient gel electrophoresis combined with sequencing analysis revealed that earthworms pronouncedly modified bacterial and fungal community structures, through broadening the community diversities of Actinobacteria, Bacteroidetes, Proteobacteria, and Ascomycotina. These results suggest that the presence of earthworms promoted the activity and population of bacteria and fungi, and modified their communities, thus altering the decomposition pathway of fresh FVW.
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http://dx.doi.org/10.1016/j.biortech.2014.07.058DOI Listing
October 2014