Trophic strategy of diverse methanogens across a river-to-sea gradient

Methanogens are an important biogenic source of methane, especially in estuarine waters across a river-to-sea gradient. However, the diversity and trophic strategy of methanogens in this gradient are not clear. In this study, the diversity and trophic strategy of methanogens in sediments across the Yellow River (YR) to the Bohai Sea (BS) gradient were investigated by high-throughput sequencing based on the 16S rRNA gene. The results showed that the diversity of methanogens in sediments varied from multitrophic communities in YR samples to specific methylotrophic communities in BS samples. The methanogenic community in YR samples was dominated by Methanosarcina, while that of BS samples was dominated by methylotrophic Methanococcoides. The distinct methanogens suggested that the methanogenic community of BS sediments did not originate from YR sediment input. High-throughput sequencing of the mcrA gene revealed that active Methanococcoides dominated in the BS enrichment cultures with trimethylamine as the substrate, and methylotrophic Methanolobus dominated in the YR enrichment cultures, as detected to a limited amount in in situ sediment samples. Methanosarcina were also detected in this gradient sample. Furthermore, the same species of Methanosarcina mazei, which was widely distributed, was isolated from the area across a river-to-sea gradient by the culture-dependent method. In summary, our results showed that a distribution of diverse methanogens across a river-to-sea gradient may shed light on adaption strategies and survival mechanisms in methanogens

Heterogeneous activation of peroxymonosulfate by a biochar-supported Co3O4 composite for efficient degradation of chloramphenicols

Herein, a new peroxymonosulfate (PMS) activation system was established using a biochar (BC)-supported Co3O4 composite (Co3O4-BC) as a catalyst to enhance chloramphenicols degradation. The effects of the amount of Co3O4 load on the BC, Co3O4-BC amount, PMS dose and solution pH on the degradation of chloramphenicol (CAP) were investigated. The results showed that the BC support could well disperse Co3O4 particles. The degradation of CAP (30 mg/L) was enhanced in the Co3O4-BC/PMS system with the apparent degradation rate constant increased to 5.1, 19.4 and 7.2 times of that in the Co3O4/PMS, BC/PMS and PMS-alone control systems, respectively. Nearly complete removal of CAP was achieved in the Co3O4-BC/PMS system under the optimum conditions of 10 wt% Co3O4 loading on BC, 0.2 g/L. Co3O4-BC, 10 mM PMS and pH 7 within 10 min. The Co3O4/BC composites had a synergistic effect on the catalytic activity possibly because the conducting BC promoted electron transfer between the Co species and HSO5- and thus accelerated the Co3+/Co(2+)redox cycle. Additionally, over 85.0 +/- 1.5% of CAP was still removed in the 10th run. Although both SO4 center dot- and OH center dot were identified as the main active species, SO4 center dot- played a dominant role in CAP degradation. In addition, two other chloramphenicols, i.e., florfenicol (FF) and thiamphenicol (TAP), were also effectively degraded with percentages of 86.4 +/- 13% and 71.8 +/- 1.0%, respectively. This study provides a promising catalyst Co3O4-BC to activate PMS for efficient and persistent antibiotics degradation. (C) 2019 Elsevier Ltd. All rights reserved

On the General Ericksen-Leslie System: Parodi's Relation, Well-posedness and Stability

In this paper we investigate the role of Parodi's relation in the well-posedness and stability of the general Ericksen-Leslie system modeling nematic liquid crystal flows. First, we give a formal physical derivation of the Ericksen-Leslie system through an appropriate energy variational approach under Parodi's relation, in which we can distinguish the conservative/dissipative parts of the induced elastic stress. Next, we prove global well-posedness and long-time behavior of the Ericksen-Leslie system under the assumption that the viscosity $\mu_4$ is sufficiently large. Finally, under Parodi's relation, we show the global well-posedness and Lyapunov stability for the Ericksen-Leslie system near local energy minimizers. The connection between Parodi's relation and linear stability of the Ericksen-Leslie system is also discussed

Circulating Cell-Free DNA in Dogs with Mammary Tumors: Short and Long Fragments and Integrity Index

Circulating cell-free DNA (cfDNA) has been considered an interesting diagnostic/prognostic plasma biomarker in tumor-bearing subjects. In cancer patients, cfDNA can hypothetically derive from tumor necrosis/apoptosis, lysed circulating cells, and some yet unrevealed mechanisms of active release. This study aimed to preliminarily analyze cfDNA in dogs with canine mammary tumors (CMTs). Forty-four neoplastic, 17 non-neoplastic disease-bearing, and 15 healthy dogs were recruited. Necrosis and apoptosis were also assessed as potential source of cfDNA on 78 CMTs diagnosed from the 44 dogs. The cfDNA fragments and integrity index significantly differentiated neoplastic versus non-neoplastic dogs (P<0.05), and allowed the distinction between benign and malignant lesions (P<0.05). Even if without statistical significance, the amount of cfDNA was also affected by tumor necrosis and correlated with tumor size and apoptotic markers expression. A significant (P<0.01) increase of Bcl-2 in malignant tumors was observed, and in metastatic CMTs the evasion of apoptosis was also suggested. This study, therefore, provides evidence that cfDNA could be a diagnostic marker in dogs carrying mammary nodules suggesting that its potential application in early diagnostic procedures should be further investigated

Deletion of BmoR affects the expression of genes related to thiol/disulfide balance in Bacteroides fragilis

Bacteroides fragilis, an opportunistic pathogen and commensal bacterium in the gut, is one the most aerotolerant species among strict anaerobes. However, the mechanisms that control gene regulation in response to oxidative stress are not completely understood. In this study, we show that the MarR type regulator, BmoR, regulates the expression of genes involved in the homeostasis of intracellular redox state. Transcriptome analysis showed that absence of BmoR leads to altered expression in total of 167 genes. Sixteen of these genes had a 2-fold or greater change in their expression. Most of these genes are related to LPS biosynthesis and carbohydrates metabolism, but there was a signifcant increase in the expression of genes related to the redox balance inside the cell. A pyridine nucleotide-disulfde oxidoreductase located directly upstream of bmoR was shown to be repressed by direct binding of BmoR to the promoter region. The expression of two other genes, coding for a thiosulphate:quinoneoxidoreductase and a thioredoxin, are indirectly afected by bmoR mutation during oxygen exposure. Phenotypic assays showed that BmoR is important to maintain the thiol/disulfde balance in the cell, confrming its relevance to B. fragilis response to oxidative stress

Gastroesophageal reflux leads to esophageal cancer in a surgical model with mice

<p>Abstract</p> <p>Background</p> <p>Esophago-gastroduodenal anastomosis with rats mimics the development of human Barrett's esophagus and esophageal adenocarcinoma by introducing mixed reflux of gastric and duodenal contents into the esophagus. However, use of this rat model for mechanistic and chemopreventive studies is limited due to lack of genetically modified rat strains. Therefore, a mouse model of esophageal adenocarcinoma is needed.</p> <p>Methods</p> <p>We performed reflux surgery on wild-type, <it>p53</it>^{<it>A</it>135<it>V </it>}transgenic, and <it>INK4a/Arf</it>^+/-mice of A/J strain. Some mice were also treated with omeprazole (1,400 ppm in diet), iron (50 mg/kg/m, <it>i.p</it>.), or gastrectomy plus iron. Mouse esophagi were harvested at 20, 40 or 80 weeks after surgery for histopathological analysis.</p> <p>Results</p> <p>At week 20, we observed metaplasia in wild-type mice (5%, 1/20) and <it>p53</it>^{<it>A</it>135<it>V </it>}mice (5.3%, 1/19). At week 40, metaplasia was found in wild-type mice (16.2%, 6/37), <it>p53</it>^{<it>A</it>135<it>V </it>}mice (4.8%, 2/42), and wild-type mice also receiving gastrectomy and iron (6.7%, 1/15). Esophageal squamous cell carcinoma developed in <it>INK4a/Arf</it>^+/-mice (7.1%, 1/14), and wild-type mice receiving gastrectomy and iron (21.4%, 3/14). Among 13 wild-type mice which were given iron from week 40 to 80, twelve (92.3%) developed squamous cell carcinoma at week 80. None of these mice developed esophageal adenocarcinoma.</p> <p>Conclusion</p> <p>Surgically induced gastroesophageal reflux produced esophageal squamous cell carcinoma, but not esophageal adenocarcinoma, in mice. Dominant negative <it>p53 </it>mutation, heterozygous loss of <it>INK4a/Arf</it>, antacid treatment, iron supplementation, or gastrectomy failed to promote esophageal adenocarcinoma in these mice. Further studies are needed in order to develop a mouse model of esophageal adenocarcinoma.</p

Role of lysophosphatidic acid receptor LPA2 in the development of allergic airway inflammation in a murine model of asthma

<p>Abstract</p> <p>Background</p> <p>Lysophosphatidic acid (LPA) plays a critical role in airway inflammation through G protein-coupled LPA receptors (LPA_1-3). We have demonstrated that LPA induced cytokine and lipid mediator release in human bronchial epithelial cells. Here we provide evidence for the role of LPA and LPA receptors in Th2-dominant airway inflammation.</p> <p>Methods</p> <p/> <p>Wild type, LPA₁heterozygous knockout mice (LPA₁^+/-), and LPA₂heterozygous knockout mice (LPA₂^+/-) were sensitized with inactivated <it>Schistosoma mansoni </it>eggs and local antigenic challenge with <it>Schistosoma mansoni </it>soluble egg Ag (SEA) in the lungs. Bronchoalveolar larvage (BAL) fluids and lung tissues were collected for analysis of inflammatory responses. Further, tracheal epithelial cells were isolated and challenged with LPA.</p> <p>Results</p> <p>BAL fluids from <it>Schistosoma mansoni </it>egg-sensitized and challenged wild type mice (4 days of challenge) showed increase of LPA level (~2.8 fold), compared to control mice. LPA₂^+/-mice, but not LPA₁^+/-mice, exposed to <it>Schistosoma mansoni </it>egg revealed significantly reduced cell numbers and eosinophils in BAL fluids, compared to challenged wild type mice. Both LPA₂^+/-and LPA₁^+/-mice showed decreases in bronchial goblet cells. LPA₂^+/-mice, but not LPA₁^+/-mice showed the decreases in prostaglandin E2 (PGE2) and LPA levels in BAL fluids after SEA challenge. The PGE2 production by LPA was reduced in isolated tracheal epithelial cells from LPA₂^+/-mice. These results suggest that LPA and LPA receptors are involved in <it>Schistosoma mansoni </it>egg-mediated inflammation and further studies are proposed to understand the role of LPA and LPA receptors in the inflammatory process.</p