Mechanisms of ammonia, calcium and heavy metal removal from nutrient-poor water by Acinetobacter calcoaceticus strain HM12.

An Acinetobacter calcoaceticus strain HM12 capable of heterotrophic nitrification-aerobic denitrification (HN-AD) under nutrient-poor conditions was isolated, with an ammonia nitrogen (NH4+-N) removal efficiency of 98.53%. It can also remove heavy metals by microbial induced calcium precipitation (MICP) with a Ca2+ removal efficiency of 75.91%. Optimal conditions for HN-AD and mineralization of the strain were determined by kinetic analysis (pH = 7, C/N = 2.0, Ca2+ = 70.0 mg L-1, NH4+-N = 5.0 mg L-1). Growth curves and nitrogen balance elucidated nitrogen degradation pathways capable of converting NH4+-N to gaseous nitrogen. The analysis of the bioprecipitation showed that Zn2+ and Cd2+ were removed by the MICP process through co-precipitation and adsorption (maximum removal efficiencies of 93.39% and 80.70%, respectively), mainly ZnCO3, CdCO3, ZnHPO4, Zn3(PO4)2 and Cd3(PO4)2. Strain HM12 produces humic and fulvic acids to counteract the toxicity of pollutants, as well as aromatic proteins to increase extracellular polymers (EPS) and promote the biomineralization process. This study provides a experimental evidence for the simultaneous removal of multiple pollutants from nutrient-poor waters.

CircANKRD17 promotes glycolysis by inhibiting miR-143 in breast cancer cells.

Glucose metabolic reprogramming, known as the Warburg effect, is one of the metabolic hallmarks of tumor cells. Cancer cells preferentially metabolize glucose by glycolysis rather than mitochondrial oxidative phosphorylation regardless of oxygen availability, but the regulatory mechanism underlying this switch has been incompletely understood. Here, we report that the circular RNA circ ankyrin repeat domain 17 (ANKRD17) functions as a key regulator for glycolysis to promote cell growth, migration, invasion, and cell-cycle progression in breast cancer (BC) cells. We further show that circANKRD17 acts to accelerate glycolysis in BC cells by acting as a sponge for miR-143 and in turn overrides the repressive effect of miR-143, a well-documented glycolytic repressor, on hexokinase 2 in BC cells, thus resulting in enhanced glycolysis in BC cells. These data suggest the circANKRD17-miR-143 cascade as a novel mechanism in controlling glucose metabolic reprogramming in BC cells and suggest circANKRD17 as a promising therapeutic target to interrupt cancerous glycolysis.

Construction of a Programmable Feedback Network with Continuously Activatable Molecular Beacon Fluorescence for One-Step Quantification of Long Noncoding RNAs in Clinical Breast Tissues.

Long noncoding RNAs (lncRNAs) are key regulators in numerous pathological and physiological processes, and their aberrant expression is implicated in many diseases. Herein, we develop a programmable feedback network with continuously activatable molecular beacon (MB) fluorescence for one-step quantification of mammalian-metastasis-associated lung adenocarcinoma transcript 1 (lncRNA MALAT1) in clinical breast tissues. We introduce a functional MB with three domains, including a substrate for lncRNA MALAT1 recognition, a template for strand displacement amplification (SDA), and a reporter for signal output with FAM fluorescence being quenched by BHQ1. When MALAT1 is present, it recognizes and unfolds the MB, leading to the recovery of FAM fluorescence. Once the MB is opened, multiple rounds of SDA reaction are automatically initiated by recruiting primer, KF DNA polymerase, and Nt.BbvCI nicking enzyme, inducing the opening of more MBs and the dissociation of more FAM/BHQ1 pairs. Consequently, a feedback network is constructed through multicycle cascade SDA, achieving the exponential accumulation of fluorescence signals for accurate quantification of MALAT1. In this assay, only two oligonucleotides (i.e., MB and primer) are involved for the establishment of a feedback amplification network, greatly simplifying the design of the reaction system. Moreover, this assay requires only one step to realize the isothermal exponential amplification for real-time monitoring of MALAT1 with attomolar sensitivity. This assay displays single-base mismatch selectivity with high anti-interference capability, and it can further quantify endogenous MALAT1 at the single-cell level and differentiate MALAT1 expression between breast cancer patient tissues and healthy person tissues.

Construction of Multiple DNAzymes Driven by Single Base Elongation and Ligation for Single-Molecule Monitoring of FTO in Cancer Tissues.

Fat mass and obesity-associated proteins (FTO) play an essential role in the reversible regulation of N6-methyladenosine (m6A) epigenetic modification, and the overexpression of FTO is closely associated with the occurrence of diverse human diseases (e.g., obesity and cancers). Herein, we demonstrate the construction of multiple DNAzymes driven by single base elongation and ligation for the single-molecule monitoring of FTO in cancer tissues. When target FTO is present, the m6A-RNA is specifically demethylated and subsequently acts as a primer to combine with the padlock probe, initiating single-base elongation and ligation reaction to generate a closed template probe. Upon the addition of phi29 DNA polymerase, a rolling circle amplification (RCA) reaction is initiated to produce large numbers of Mg2+-dependent DNAzyme repeats. Subsequently, the DNAzymes cyclically digest the signal probes, liberating numerous Cy5 molecules that can be precisely counted by single-molecule imaging. Taking advantage of the sequence specificity of the polymerase/ligase-mediated gap-filling and ligation as well as the high amplification efficiency of RCA, this biosensor shows excellent specificity and high sensitivity with a detection limit of 5.96 × 10-16 M. It can be applied to screen FTO inhibitors and quantify FTO activity at the single-cell level. Moreover, the proposed strategy can accurately distinguish the FTO expression level in tissues of healthy individuals and breast cancer patients, providing a new platform for drug discovery, m6A modification-related research, and clinical diagnostics.

PHB regulates meiotic recombination via JAK2-mediated histone modifications in spermatogenesis.

Previously, we have shown that human sperm Prohibitin (PHB) expression is significantly negatively correlated with mitochondrial ROS levels but positively correlated with mitochondrial membrane potential and motility. However, the possible role of PHB in mammalian spermatogenesis has not been investigated. Here we document the presence of PHB in spermatocytes and its functional roles in meiosis by generating the first male germ cell-specific Phb-cKO mouse. Loss of PHB in spermatocytes resulted in complete male infertility, associated with not only meiotic pachytene arrest with accompanying apoptosis, but also apoptosis resulting from mitochondrial morphology and function impairment. Our mechanistic studies show that PHB in spermatocytes regulates the expression of STAG3, a key component of the meiotic cohesin complex, via a non-canonical JAK/STAT pathway, and consequently promotes meiotic DSB repair and homologous recombination. Furthermore, the PHB/JAK2 axis was found as a novel mechanism in the maintenance of stabilization of meiotic STAG3 cohesin complex and the modulation of heterochromatin formation in spermatocytes during meiosis. The observed JAK2-mediated epigenetic changes in histone modifications, reflected in a reduction of histone 3 tyrosine 41 phosphorylation (H3Y41ph) and a retention of H3K9me3 at the Stag3 locus, could be responsible for Stag3 dysregulation in spermatocytes with the loss of PHB.

Two MicroRNAs, miR-34a and miR-125a, Are Implicated in Bicuspid Aortopathy by Modulating Metalloproteinase 2.

It has been recognized that wall shear stress plays an important role in the development of Bicuspid Aortopathy (BA), but the intrinsic mechanism is not well elucidated. This study aims to explore the underlying relationship between hemodynamical forces and pathological phenomenon. Total RNA was prepared from aortic wall tissues collected from 20 BA patients. RNA sequencing, bioinformatic analysis and quantitative reverse-transcription PCR validation identified nine miRNAs that were up-regulated in the aortic part exposed to high wall shear stress compared to the low wall shear stress control, and six miRNAs that were down-regulated. Among these candidates, miR-34a and miR-125a, both down-regulated in the high wall shear stress parts, were shown to be potential inhibitors of the metalloproteinase 2 gene. Luciferase reporter assays confirmed that both miRNAs could inhibit the expression of metalloproteinase 2 mRNA in CRL1999 by complementing with its 3' untranslated region. Conversely, immunofluorescence assays showed that inhibition of miR-34a or miR-125a could lead to increased metalloproteinase 2 protein level. On the other hand, both miR-34a and miR-125a were shown to alleviate stretch-induced stimulation of metalloproteinase 2 expression in CRL1999 cells. The results suggested that miR-34a and miR-125a might be implicated in wall shear stress induced aortic pathogenesis due to their apparent regulatory roles in metalloproteinase 2 expression and extracellular matrix remodeling, which are key events in the weakening of aortic walls among BA patients.

Suppression of miR-199a maturation by HuR is crucial for hypoxia-induced glycolytic switch in hepatocellular carcinoma.

Glucose metabolic reprogramming is a hallmark of cancer. Cancer cells rapidly adjust their energy source from oxidative phosphorylation to glycolytic metabolism in order to efficiently proliferate in a hypoxic environment, but the mechanism underlying this switch is still incompletely understood. Here, we report that hypoxia potently induces the RNA-binding protein HuR to specifically bind primary miR-199a transcript to block miR-199a maturation in hepatocellular carcinoma (HCC) cells. We demonstrate that this hypoxia-suppressed miR-199a plays a decisive role in limiting glycolysis in HCC cells by targeting hexokinase-2 (Hk2) and pyruvate kinase-M2 (Pkm2). Furthermore, systemically delivered cholesterol-modified agomiR-199a inhibits [(18)F]-fluorodeoxyglucose uptake and attenuates tumor growth in HCC tumor-bearing mice. These data reveal a novel mechanism of reprogramming of cancer energy metabolism in which HuR suppresses miR-199a maturation to link hypoxia to the Warburg effect and suggest a promising therapeutic strategy that targets miR-199a to interrupt cancerous aerobic glycolysis.

MicroRNA regulation and analytical methods in cancer cell metabolism.

The reprogramming of glucose metabolism from oxidative to glycolytic metabolism, known as the Warburg effect, is an anomalous characteristic of cancer cell metabolism. Recent studies have revealed a subset of microRNAs (miRNAs) that play critical roles in regulating the reprogramming of glucose metabolism in cancer cells. These miRNAs regulate cellular glucose metabolism by directly targeting multiple metabolic genes, including those encoding key glycolytic enzymes. In the first part of this review, we summarized the recent knowledge of miRNA regulation in the reprogramming of glucose metabolism in cancer cells and discussed the potential utilization of the key miRNA regulators as metabolic targets for developing new antitumor agents. Then, we summarized recent advances in methods and techniques for studying miRNA regulation in cancer cell metabolism.

A novel miR-155/miR-143 cascade controls glycolysis by regulating hexokinase 2 in breast cancer cells.

Cancer cells preferentially metabolize glucose through aerobic glycolysis. This phenomenon, known as the Warburg effect, is an anomalous characteristic of glucose metabolism in cancer cells. Chronic inflammation is a key promoting factor of tumourigenesis. It remains, however, largely unexplored whether and how pro-tumourigenic inflammation regulates glucose metabolism in cancer cells. Here, we show that pro-inflammatory cytokines promote glycolysis in breast cancer cells, and that the inflammation-induced miR-155 functions as an important mediator in this process. We further show that miR-155 acts to upregulate hexokinase 2 (hk2), through two distinct mechanisms. First, miR-155 promotes hk2 transcription by activation of signal transducer and activator of transcription 3 (STAT3), a transcriptional activator for hk2. Second, via targeting C/EBPß (a transcriptional activator for mir-143), miR-155 represses mir-143, a negative regulator of hk2, thus resulting in upregulation of hk2 expression at the post-transcriptional level. The miR-155-mediated hk2 upregulation also appears to operate in other types of cancer cells examined. We suggest that the miR-155/miR-143/HK2 axis may represent a common mechanism linking inflammation to the altered metabolism in cancer cells.

Ammonium nitrogen and phosphorus removal by bacterial-algal symbiotic dynamic sponge bioremediation system in micropolluted water: Operational mechanism and transformation pathways.

Construct a bacteria-algae symbiotic dynamic sponge bioremediation system to simultaneously remove multiple pollutants under micro-pollution conditions. The average removal efficiencies of NH4+-N, PO43--P, total nitrogen (TN), and Ca2+ were 98.35, 78.74, 95.64, and 84.92 %, respectively. Comparative studies with Auxenochlorella sp. sponge and bacterial sponge bioremediation system confirmed that NH4+-N and TN were mainly removed by bacterial heterotrophic nitrification - aerobic denitrification (HN-AD). PO43--P was removed by algal assimilation and the generation of Ca3(PO4)2 and Ca5(PO4)3OH, and Ca2+ was removed by algal electron transfer formation of precipitates and microbially induced calcium precipitation (MICP) by bacteria. Algae provided an aerobic environment for the bacterial HN-AD process through photosynthesis, while respiration produced CO2 and adsorbed Ca2+ to promote the formation of calcium precipitates. Immobilization of Ca2+ with microalgae via bacterial MICP helped to lift microalgal photoinhibition. The bioremediation system provides theoretical support for research on micropolluted water treatment while increasing phosphorus recovery pathways.

Loofah sponge crosslinked polyethyleneimine loaded with biochar biofilm reactor for ecological remediation of oligotrophic water: Mechanism, performance, and functional characterization.

The removal of complex pollutants from oligotrophic water is an important challenge for researchers. In this study, the HCl-modified loofah sponge crosslinked polyethyleneimine loaded with biochar (LS/PEI@biochar) biofilm reactor was adapted to achieve efficient removal of complex pollutants in oligotrophic water. On the 35 d, the average removal efficiency of chemical oxygen demand (COD), ammonia nitrogen (NH4+-N), calcium (Ca2+), and phosphate (PO43--P) in water was 51, 95, 81, and 77 %, respectively. Additionally, it effectively used a low molecular weight carbon source. Scanning electron microscopy (SEM) results showed that the LS/PEI@biochar biocarrier had superior biofilm suspension performance. Meanwhile, analysis of the biocrystals confirmed Ca2+ and PO43- removal through the generation of CaCO3 (calcite and vaterite) and Ca5(PO4)3OH. This study demonstrated that the system has great efficiency and application prospect in treating oligotrophic water on the laboratory scale, and will be further validated for practical application on large-scale oligotrophic water.

Simultaneous removal of phosphate, calcium, and ammonia nitrogen in a hydrogel immobilized reactor with bentonite/lanthanum/PVA based on microbial induced calcium precipitation.

In recent years, it is urgent to solve nitrogen and phosphorus pollution in domestic wastewater. The target strain Pseudomonas sp. Y1 was immobilized using polyvinyl alcohol (PVA) matrix coupled with bentonite and lanthanum (La), respectively, to fabricate four hydrogel materials that used to construct bioreactors. The optimal operating parameters and dephosphorization mechanism were discussed, and the effects of hydrogel materials and different loads on the performance of the bioreactor were contrastively analyzed. The results manifested that when the hydraulic retention time (HRT) was 6.0 h, the C/N was 6.0, and the Ca2+ concentration was 100.0 mg L-1, the bioreactors had the best heterotrophic nitrification-aerobic denitrification (HNAD) and biomineralization capacity, and the maximum removal efficiencies of Ca2+, PO43--P, and NH4+-N were 82.57, 99.17, and 89.08%, respectively. The operation data indicated that the addition of bentonite significantly promoted HNAD, and the bioreactor had stronger dephosphorization ability in the presence of La. The main phosphorous removal mechanisms were confirmed to be adsorption and co-precipitation. Finally, high-throughput sequencing results indicated that Pseudomonas accounted for the paramount proportion in the bioreactor, and the prediction of functional genes indicated that the C/N of 6.0 is more favorable for the expression of nitrogen removal-related functional genes in the bioreactor system. This study highlights the superiority of microbial induced calcium precipitation (MICP) combined with PVA hydrogel, and provides a theoretical basis for simultaneous nitrogen and phosphate removal of wastewater.

Label-free and sensitive detection of N6-methyladenosine demethylase activity in crude cell extracts and clinical cancer tissues based on demethylation-triggered exponential signal amplification.

The m6A demethylase catalyzes the removal of m6A modification to establish proper RNA methylation patterns, and it has emerged as a promising disease biomarker and a therapeutic target. The reported m6A demethylase assays often suffer from tedious producers, expensive reagents, radioactive risk, limited sensitivity, and poor specificity. Herein, we develop a simple, selective, label-free, and highly sensitive fluorescent biosensor for m6A demethylase assay based on demethylation-triggered exponential signal amplification. In this biosensor, m6A demethylase-catalyzed demethylation can protect the circular DNA from the digestion by DpnI, subsequently triggering hyperbranched rolling circle amplification to achieve exponential signal amplification for producing abundant ssDNA and dsDNA products. The amplified DNA signal can be sensitively and simply detected by SYBR Gold in a label-free manner. This biosensor avoids any antibodies, washing/separation procedures, and fluorophore-/quencher-labeled probes, great simplifying the assay procedures and reducing the assay cost. Moreover, this biosensor achieves good specificity and excellent sensitivity with a detection limit of 1.2 fg/µL, which is superior to conventional ELISA (36.3 pg/µL). Especially, this biosensor enables direct monitoring of m6A demethylase activity in crude cell extracts with high accuracy, and it can be further applied for the screening of m6A demethylase inhibitor, measurement of m6A demethylase activity in different cell lines, and discrimination of m6A demethylase level in clinical cancer and healthy tissues, providing a facile and robust platform for RNA methylation-related biomedical research, disease diagnosis, and drug discovery.

Microencapsulated reactor for simultaneous removal of calcium, fluoride and phenol using microbially induced calcium precipitation: Mechanism and functional characterization.

Fluoride ions (F-) and phenol in groundwater have become a great hurdle to the pursuit of a healthy drinking water source. This study established a microencapsulated immobilization reactor with Aquabacterium sp. CZ3 for the simultaneous removal of nitrate (NO3--N), calcium (Ca2+), F-, and phenol from groundwater with 100%, 67.84%, 88.67%, and 100% removal efficiencies, respectively. The three-dimensional mesh structure of microcapsules facilitated the transport and metabolism of substances, while their synergistic effect with bacteria promoted the removal of contaminants. F- was removed by co-precipitation to generate Ca5(PO4)3F and CaF2 and adsorption. On one hand, the phenol toxicity promoted the production of extracellular polymers and improved the tolerance of bacteria; on the other hand, the degradation of phenol provided a carbon source for bacteria and promoted the denitrification. The development of microencapsulated immobilized reactor provided a clear mechanism for phenol and F- removal under the microbially induced calcium precipitation (MICP) technique, while providing a valuable solution for the treatment of complex groundwater resources.

Venous and Arterial Thromboembolism in Patients with Metastatic Lung Cancer.

Lung cancer is the leading cause of cancer-related mortality worldwide with an increasing incidence in many countries. There were few studies on arterial and venous thromboembolism (ATE/VTE) in patients with metastatic lung cancer. Our study focused on the clinical characteristics of stage IV lung cancer patients with ATE or VTE to further explore the risk factors and prognosis. Patients diagnosed with metastatic lung cancer were enrolled from January 2011 to June 2019 at a tertiary hospital in Jiangyin, China. Log-rank test was used to reveal the survival for patients with ATE or VTE. Univariable analysis and multivariable logistic regression were used to study the risk factors for ATE. A total of 587 patients were enrolled in our study, including 52 patients with VTE and 48 with ATE. ATE occurred earlier than VTE. Patients with ATE had a worse prognosis. Multivariable logistic regression revealed that older age and a history of hypertension were independent risk factors for ATE. Patients with metastatic lung cancer were at high risk of VTE and ATE. ATE occurred earlier and was associated with a worse prognosis. Attention should be paid to metastatic lung cancer patients who may develop thromboembolism, especially ATE.

Verteporfin Suppresses YAP-Induced Glycolysis in Breast Cancer Cells.

OBJECTIVE: The inhibition of the Hippo pathway through targeting the Yes-associated protein (YAP) presents a novel and promising approach for treating tumors. However, the efficacy of YAP inhibitors in the context of breast cancer (BC) remains incompletely understood. Here, we aimed to investigate the involvement of YAP in BC's metabolic reprogramming and reveal the potential underlying mechanisms. To this end, we assessed the function of verteporfin (VP), a YAP-TEAD complex inhibitor, on the glycolytic activity of BC cells. METHODS: We evaluated the expression of YAP by utilizing immunohistochemistry (IHC) in BC patients who have undergone 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) prior to biopsy/surgery. We employed RNA immunoprecipitation (RIP) and fluorescent in situ hybridization (FISH) assays to assess the interaction between YAP mRNA and human antigen R (HuR) in BC cells. The biological importance of YAP in the metabolism and malignancy of BC was evaluated in vitro. Finally, the effect of VP on glycolysis was determined by using 18F-FDG uptake, glucose consumption, and lactate production assays. RESULTS: Our studies revealed that high expression of YAP was positively correlated with the maximum uptake value (SUVmax) determined by 18F-FDG PET/CT imaging in BC samples. Inhibition of YAP activity suppressed glycolysis in BC. The mechanism underlying this phenomenon could be the binding of YAP to HuR, which promotes glycolysis in BC cells. Treatment with VP effectively suppressed glycolysis induced by YAP overexpression in BC cells. CONCLUSION: VP exhibited anti-glycolytic effect on BC cells, indicating its therapeutic value as an FDA-approved drug.

A novel microRNA-182/Interleukin-8 regulatory axis controls osteolytic bone metastasis of lung cancer.

Bone metastasis is one of the main complications of lung cancer and most important factors that lead to poor life quality and low survival rate in lung cancer patients. However, the regulatory mechanisms underlying lung cancer bone metastasis are still poor understood. Here, we report that microRNA-182 (miR-182) plays a critical role in regulating osteoclastic metastasis of lung cancer cells. We found that miR-182 was significantly upregulated in both bone-metastatic human non-small cell lung cancer (NSCLC) cell line and tumor specimens. We further demonstrated that miR-182 markedly enhanced the ability of NSCLC cells for osteolytic bone metastasis in nude mice. Mechanistically, miR-182 promotes NSCLC cells to secrete Interleukin-8 (IL-8) and in turn facilitates osteoclastogenesis via activating STAT3 signaling in osteoclast progenitor cells. Importantly, systemically delivered IL-8 neutralizing antibody inhibits NSCLC bone metastasis in nude mice. Collectively, our findings identify the miR-182/IL-8/STAT3 axis as a key regulatory pathway in controlling lung cancer cell-induced osteolytic bone metastasis and suggest a promising therapeutic strategy that targets this regulatory axis to interrupt lung cancer bone metastasis.

Rapid and label-free monitoring of exonuclease III-assisted target recycling amplification.

Target recycling-oriented amplification has been widely applied for sensitive detection of DNA, RNA, and proteins due to its successful overcoming the inherent limitation of target-to-signal ratio of 1:1 in the traditional hybridization assay. Exonuclease III (Exo III) is usually used as the cleavage enzyme in the target recycling-oriented amplification because of its easy availability, high catalytic activity, and wide applicability. Even though Exo III is assumed to be double-stranded DNA (dsDNA) specific exonuclease in most literature, its cleavage of single-strand DNA (ssDNA) does occur, resulting in the target-independent degradation of probes. Herein, we design an intramolecular displacement probe with the capability of resistance to the nonspecific digestion of Exo III and fast hybridization kinetics. Through the substitution of 2-aminopurine for adenine in the intramolecular displacement probes, we develop a rapid and label-free approach to monitor Exo III-assisted target recycling amplification. We further demonstrate that this method can be used for the detection of DNA and proteins with excellent specificity and high sensitivity. Importantly, this method can be extended to rapid, label-free and multiplexed detection of various nucleic acids, proteins, and small molecules using different kinds of fluorescent nucleotide analogues and specific aptamers.

Single quantum dot based nanosensor for renin assay.

Evaluation of plasma renin activity is essential to the assessment of renin-related diseases such as hypertension, congestive heart failure, and cancers. Here, we develop a single quantum dot (QD) based nanosensor for sensitive detection of renin activity. This single-QD-based nanosensor consists of a streptavidin-coated QD and multiple biotinylated and Cy5-labeled peptide substrates, which form a QD/substrate/Cy5 complex where fluorescence resonance energy transfer (FRET) occurs with the QD as the donor and Cy5 as the acceptor. The presence of renin leads to the cleavage of the substrate and the separation of Cy5 from the QD and consequently the decrease of FRET efficiency and the reduction of Cy5 counts. Through the measurement of Cy5 counts by total internal reflection fluorescence (TIRF) microscopy, the renin activity can be quantitatively evaluated at the single-molecule level. This single-QD-based nanosensor can measure not only the renin concentration, but also the enzymatic velocity and the Michaelis-Menten kinetic parameters, and has significant advantages of simplicity, low cost with minimum sample consumption, and high sensitivity with a detection limit of 25 pM. This single-QD-based nanosensor might be further applied to monitor a variety of important enzymatic biomarkers such as kinases and endonuleases.

Biocatalytic synthesis of poly(δ-valerolactone) using a thermophilic esterase from archaeoglobus fulgidus as catalyst.

The ring-opening polymerization of δ-valerolactone catalyzed by a thermophilic esterase from the archaeon Archaeoglobus fulgidus was successfully conducted in organic solvents. The effects of enzyme concentration, temperature, reaction time and reaction medium on monomer conversion and product molecular weight were systematically evaluated. Through the optimization of reaction conditions, poly(δ-valerolactone) was produced in 97% monomer conversion, with a number-average molecular weight of 2225 g/mol, in toluene at 70 °C for 72 h. This paper has produced a new biocatalyst for the synthesis of poly(δ-valerolactone), and also deeper insight has been gained into the mechanism of thermophilic esterase-catalyzed ring-opening polymerization.