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Anaerobic ammonium oxidation (anammox) is a process of ammonium and nitrite conversion into nitrogen gas. Nowadays, anammox is applied into many wastewater treatment plants worldwide. However, anammox bacteria are characterized by a slow growth rate, which may cause problems in maintaining the biomass in the system. The promising technique which can help to maintain the biomass in the reactor and effectively prevent loss of anammox bacteria from a system is immobilization. Selection and optimization of the appropriate immobilization technique for investigated biomass is crucial for conducting an effective process. One of the ways for bacteria immobilization is gel entrapment. The main goal of the study was to test sodium alginate as an immobilization medium for anammox biomass. In the present study procedure of immobilization in sodium alginate was optimised, then the mechanical and chemical properties of the obtained pellets were investigated. Series of batch experiments revealed that immobilized anammox biomass was able to remove ammonia and nitrite nitrogen effectively. The calculated specific anammox activity (SAA) for immobilized anammox biomass was 0.18 g N·gVSS-1·d-1, while for non-immobilized biomass was 0.36 g N·gVSS-1·d-1.

More information on the connection between anaerobic digestion (AD) parameters and composition of the microbial community involved in the AD process is required to gain a better understanding of how a bioreactor functions. The aim of this study was to analyse the composition of microbial communities and the dynamics of methanogens' biodiversity changes during the shift from mesophilic (38°C) to thermophilic (55°C) conditions during biogas production. The total microbial composition was examined via the metagenomic approach based on 16S rRNA gene sequencing, whereas the methanogen communities were analysed using PCR–DGGE (Polymerase Chain Reaction–Denaturing Gradient Gel Electrophoresis) of mcrA. Even though the temperature is one of the crucial parameters affecting microorganisms involved in the AD process, the results presented here revealed that there were no statistically significant differences in bacterial community composition between the mesophilic and thermophilic phases of the process. The most abundant phyla were found to be Proteobacteria, Firmicutes, Actinobacteria and Bacteroidetes. However, the methanogens' community genotypic structure as examined by the PCR–DGGE method changed under thermophilic conditions. The temperature had the strongest impact on the archaeal methanogens in the fermentation chamber directly after implementing the temperature shift. A relatively higher biogas yield and average content of CH4 in the produced biogas were observed under thermophilic conditions. [ABSTRACT FROM AUTHOR]

This work presents a synthesis of new group of unsymmetrical chiral tellurides obtained in the reaction of sodium methanetellurolate or sodium benzenetellurolate with appropriate terpenyl tosylates from p-menthane, carane, and pinane systems. Additionally, symmetrical diterpenyl tellurides were prepared according to our recently published method using sodium telluride and terpenyl tosylates. Methyl terpenyl, phenyl terpenyl, and diterpenyl tellurides were successfully used in tellurium ylide-mediated asymmetric epoxidation reaction. The best result of asymmetric epoxidation was obtained for dicaranyl telluride (d.r. cis:trans 11:89, e.r. trans 84:16). [ABSTRACT FROM PUBLISHER]

Synthesis of terpenyl selenides derived from limonene, menthol, caranol, and myrtanol is described. Three methodologies for the synthesis of terpenyl selenonium salts are compared. The results of selenium-mediated epoxidation through the use of isoselenocineole derived from limonene and methyl terpenyl, phenyl terpenyl, diterpenyl selenides, and selenonium salts are presented. The influence of solvent, counteranion, and diastereomeric purity of selenonium salt on the enantioselectivity of the epoxidation reaction is discussed. [ABSTRACT FROM AUTHOR]

Convenient routes for the synthesis of optically active methyl, phenyl, and dimonoterpenyl sulfides derived from carane,p-menthane, pinane, and bornane were developed. Methyl and dimonoterpenyl sulfides have been obtained by the reaction of the corresponding monoterpene thiolates with methyl iodide or monoterpene tosylates. The reactions of monoterpene tosylates with sodium benzenethiolate gave the corresponding phenyl monoterpenyl sulfides. These sulfides were used for the sulfur ylide-mediated reaction to yield epoxides. Good diastereoselectivities up to 99:1 and low to moderate enantioselectivities were observed for the enantioselective synthesis of chiral epoxides. [ABSTRACT FROM PUBLISHER]

The asymmetric base-promoted coupling of benzaldehyde and benzyl bromide to 1,2-diphenyloxirane is investigated in the presence of a variety (24 examples) of terpene derived selenides as chiral mediator or catalyst. [ABSTRACT FROM AUTHOR]

Educational Objective: At the conclusion of this presentation, the participants should be able to discuss the concepts of autophagy and tumor cell dormancy, and how these cellular processes may be targeted in order to prolong survival in patients with squamous cell carcinoma of the head and neck. Objective: (1) To explain the concept of tumor cell dormancy (2) To define the role of autophagy, which is a form of nutrient recycling, as a mechanism by which dormant tumor cells survive nutrient deprivation 3) To identify a molecular pathway responsible for the induction of autophagy. Study Design / Methods: In vivo laboratory study using the HEp3 cell line. Results: Dormant HEp3 (DHEp3) cells had a significantly higher baseline level of autophagy as compared to tumorigenic HEp3 (THEp3) cells. DHEp3 cells also had higher viability rates after treatment with chloroquine. Activation of pERK in THEp3 cells increased autophagy, while deactivation of pERK in DHEp3 cells decreased autophagy. Conclusion: Pharmacological inhibition of autophagy or the pERK pathway may prolong survival in patients with locally advanced head and neck cancer. [ABSTRACT FROM AUTHOR]

Upregulation of matrix metalloproteinase MMP-14 (MT1-MMP) is associated with poor prognosis in cancer patients, but it is unclear how MMP-14 becomes elevated in tumors. Here, we show that miR-181a-5p is downregulated in aggressive human breast and colon cancers where its levels correlate inversely with MMP-14 expression. In clinical specimens, enhanced expression of MMP-14 was observed in cancer cells located at the invasive front of tumors where miR-181a-5p was downregulated relative to adjacent normal cells. Bioinformatics analyses defined a potential miR-181a-5p response element within the 30-untranslated region of MMP-14 that was validated in reporter gene experiments. Ectopic miR-181a-5p reduced MMP-14 expression, whereas miR-181a-5p attenuation elevated MMP-14 expression. In support of a critical relationship between these two genes, miR-181a-5p-mediated reduction of MMP-14 levels was sufficient to decrease cancer cell migration, invasion, and activation of pro-MMP-2. Furthermore, this reduction in MMP-14 levels was sufficient to reduce in vivo invasion and angiogenesis in chick chorioallantoic membrane assays. Taken together, our results establish the regulation of MMP-14 in cancers by miR-181a-5p through a posttranscriptional mechanism, and they further suggest strategies to elevate miR-181a-5p to prevent cancer metastasis. [ABSTRACT FROM AUTHOR]

Keratins that are overexpressed selectively in human carcinomas may offer diagnostic and prognostic utility. In this study, we show that high expression of keratin-17 (K17) predicts poor outcome in patients with cervical cancer, at early or late stages of disease, surpassing in accuracy either tumor staging or loss of p27KIP1 as a negative prognostic marker in this setting. We investigated the mechanistic basis for the biologic impact of K17 through loss- and gain-of-function experiments in human cervix, breast, and pancreatic cancer cells. Specifically, we determined that K17 functions as an oncoprotein by regulating the subcellular localization and degradation of p27KIP1. We found that K17 was released from intermediate filaments and translocated into the nucleus via a nuclear localization signal (NLS), specific among keratins, where it bound p27KIP1 during G1 phase of the cell cycle. p27KIP1 lacks a nuclear export signal (NES) and requires an adaptor for CRM1 binding for nuclear export. In K17, we defined and validated a leucine-rich NES that mediated CRM1 binding for export. Cervical cancer cells expressing K17 mutations in its NLS or NES signals exhibited an increase in levels of nuclear p27KIP1, whereas cells expressing wild-type K17 exhibited a depletion in total endogenous p27KIP1. In clinical specimens of cervical cancer, we confirmed that the expressions of K17 and p27KIP1 were inversely correlated, both across tumors and within individual tumors. Overall, our findings establish that K17 functions specially among keratins as an oncoprotein by controlling the ability of p27KIP1 to influence cervical cancer pathogenesis. [ABSTRACT FROM AUTHOR]

Cell migration-inducing protein (CEMIP) and binding immunoglobulin protein (BiP) are upregulated in human cancers, where they drive cancer progression and metastasis. It has been shown that CEMIP resides in the endoplasmic reticulum (ER) where it interacts with BiP to induce cell migration, but the relationship between the two proteins was previously unknown. Here we show that CEMIP mediates activation of the BiP promoter and upregulates BiP transcript and protein levels in breast cancer cell lines. Moreover, CEMIP overexpression confers protective adaptations to cancer cells under hypoxic conditions, by decreasing apoptosis, activating autophagy, and increasing glucose uptake, to facilitate tumor growth. We demonstrate that BiP signals downstream of CEMIP, modulating cellular resistance to hypoxia. Reducing BiP in CEMIP-expressing cells sensitized cells to hypoxia treatment, decreased glucose uptake, and resulted in tumor regression in vivo . Our study provides insights into the link between CEMIP and BiP expression and the pro-survival role they play in hypoxia. Better understanding of the mechanisms behind cancer cell adaptations to harsh tumor environments could lead to development of improved cancer treatments., Competing Interests: CONFLICTS OF INTEREST The authors declare no conflicts of interest.

Matrix metalloproteinases (MMPs) play critical roles in cancer invasion and metastasis by digesting basement membrane and extracellular matrix (ECM). Much attention has focused on the enzymatic activities of MMPs; however, the regulatory mechanism of MMP expression remains elusive. By employing bioinformatics analysis, we identified a potential p53 response element within the MMP-14 promoter. Experimentally, we found that p53 can repress MMP-14 promoter activity, whereas deletion of this p53 response element abrogated this effect. Furthermore, we found that p53 expression decreases MMP-14 mRNA and protein levels and attenuates MMP-14-mediated cellular functions. Additional promoter analysis and chromatin immunoprecipitation studies identified a mechanism of regulation of MMP-14 expression by which p53 and transcription factor Sp1 competitively bind to the promoter. As the correlation between inflammation and cancer aggressiveness is well described, we next sought to evaluate if inflammatory cytokines could differentially affect p53 and MMP-14 levels. We demonstrate that interleukin-6 (IL-6) down-regulates p53 protein levels and thus results in a concomitant increase in MMP-14 expression, leading to enhanced cancer cell invasion and metastasis. Our data collectively indicate a novel mechanism of regulation of MMP-14 by a cascade of IL-6 and p53, demonstrating that the tumor microenvironment directly stimulates molecular changes in cancer cells to drive an invasive phenotype., Competing Interests: The authors declare that they have no conflicts of interest with the contents of this article.

Keratins that are overexpressed selectively in human carcinomas may offer diagnostic and prognostic utility. In this study, we show that high expression of keratin-17 (K17) predicts poor outcome in patients with cervical cancer, at early or late stages of disease, surpassing in accuracy either tumor staging or loss of p27(KIP1) as a negative prognostic marker in this setting. We investigated the mechanistic basis for the biologic impact of K17 through loss- and gain-of-function experiments in human cervix, breast, and pancreatic cancer cells. Specifically, we determined that K17 functions as an oncoprotein by regulating the subcellular localization and degradation of p27(KIP1). We found that K17 was released from intermediate filaments and translocated into the nucleus via a nuclear localization signal (NLS), specific among keratins, where it bound p27(KIP1) during G1 phase of the cell cycle. p27(KIP1) lacks a nuclear export signal (NES) and requires an adaptor for CRM1 binding for nuclear export. In K17, we defined and validated a leucine-rich NES that mediated CRM1 binding for export. Cervical cancer cells expressing K17 mutations in its NLS or NES signals exhibited an increase in levels of nuclear p27(KIP1), whereas cells expressing wild-type K17 exhibited a depletion in total endogenous p27(KIP1). In clinical specimens of cervical cancer, we confirmed that the expressions of K17 and p27(KIP1) were inversely correlated, both across tumors and within individual tumors. Overall, our findings establish that K17 functions specially among keratins as an oncoprotein by controlling the ability of p27(KIP1) to influence cervical cancer pathogenesis., (©2015 American Association for Cancer Research.)

Hypoxic stress drives cancer progression by causing a transcriptional reprogramming. Recently, KIAA1199 was discovered to be a cell-migration inducing protein (renamed CEMIP) that is upregulated in human cancers. However, the mechanism of induction of CEMIP in cancer was hitherto unknown. Here we demonstrate that hypoxia induces CEMIP expression leading to enhanced cell migration. Immunohistochemistry of human colon cancer tissues revealed that CEMIP is upregulated in cancer cells located at the invasive front or in the submucosa. CEMIP localization inversely correlated with E-cadherin expression, which is characteristic of the epithelial-to-mesenchymal transition. Mechanistically, hypoxia-inducible-factor-2α (HIF-2α), but not HIF-1α binds directly to the hypoxia response element within the CEMIP promoter region resulting in increased CEMIP expression. Functional characterization reveals that CEMIP is a downstream effector of HIF-2α-mediated cell migration. Expression of CEMIP was demonstrated to negatively correlate with the expression of Jarid1A, a histone demethylase that removes methyl groups from H3K4me3 (an activation marker for transcription), resulting in altered gene repression. Low oxygen tension inhibits the function of Jarid1A, leading to increased presence of H3K4me3 within the CEMIP promoter. These results provide insight into the upregulation of CEMIP within cancer and can lead to novel treatment strategies targeting this cancer cell migration-promoting gene.

Upregulation of matrix metalloproteinase MMP-14 (MT1-MMP) is associated with poor prognosis in cancer patients, but it is unclear how MMP-14 becomes elevated in tumors. Here, we show that miR-181a-5p is downregulated in aggressive human breast and colon cancers where its levels correlate inversely with MMP-14 expression. In clinical specimens, enhanced expression of MMP-14 was observed in cancer cells located at the invasive front of tumors where miR-181a-5p was downregulated relative to adjacent normal cells. Bioinformatics analyses defined a potential miR-181a-5p response element within the 3'-untranslated region of MMP-14 that was validated in reporter gene experiments. Ectopic miR-181a-5p reduced MMP-14 expression, whereas miR-181a-5p attenuation elevated MMP-14 expression. In support of a critical relationship between these two genes, miR-181a-5p-mediated reduction of MMP-14 levels was sufficient to decrease cancer cell migration, invasion, and activation of pro-MMP-2. Furthermore, this reduction in MMP-14 levels was sufficient to reduce in vivo invasion and angiogenesis in chick chorioallantoic membrane assays. Taken together, our results establish the regulation of MMP-14 in cancers by miR-181a-5p through a posttranscriptional mechanism, and they further suggest strategies to elevate miR-181a-5p to prevent cancer metastasis., (©2015 American Association for Cancer Research.)