Quantitatively deciphering the roles of sediment nitrogen removal in environmental and climatic feedbacks in two subtropical estuaries.

Sedimentary denitrification and anaerobic ammonium oxidation (anammox) are two microbially-mediated nitrogen removal pathways with distinct climatic feedbacks. Estuaries receive large fluxes of anthropogenic nitrogen and serve as hotspots for nitrogen loss. Applying 15N isotope pairing technique and sediment intact core incubation in two subtropical estuaries, the Yangtze River Estuary (YRE) and Jiulong River Estuary (JRE), we show that denitrification predominates the sedimentary nitrogen loss with a minor contribution (8.6 ± 7.5%) from anammox. Particulate organic matter degradation sustains the sedimentary nitrogen removal linking the nitrogen transformations between water column and sediment. Our results indicate that estuarine sediments exhibit high areal nitrogen removal rate, but play a relatively weak role in eliminating the nitrogen inputted from river basin due to the limited area. The riverine excess nitrogen will eventually enter into the adjacent continental shelf and be removed via phytoplankton assimilation-sedimentation-degradation-coupled nitrification-denitrification. In addition, sedimentary denitrification causes 1.8 ± 2.2% of nitrogen flow towards nitrous oxide (N2O) production and the derived N2O release flux accounts for 59% and 65% of the daily sea-air N2O emission in the YRE and JRE, respectively. These findings contribute to a better understanding of estuarine sedimentary nitrogen removal and associated climate feedbacks, and to the parameterization of Earth system models.

Stem cell transplantation for treating liver diseases: progress and remaining challenges.

With the development of regenerative medicine, various stem cells are increasingly considered for treating liver diseases. Various stem cells have been reported to play an essential role in liver recovery, and studies have verified the preliminary effectiveness and safety of these therapies. Stem cell-based therapies will emerge as an effective treatment strategy for liver diseases. Thus, the research progress and challenges to the related stem cells were reviewed, namely the classification of stem cells, cell culture, transplantation, cell tracing in the body, therapies for various liver diseases.

Transplanted mouse liver stem cells at different stages of differentiation ameliorate concanavalin A-induced acute liver injury by modulating Tregs and Th17 cells in mice.

Acute liver failure (ALF) is a disease with a considerably high mortality rate that still lacks a safe and effective treatment. Transplantation of liver stem cells (LSCs) has been considered to be a promising therapeutic alternative for ALF since LSCs have been shown to be involved in immunomodulation and functional reconstruction of the liver. Our present study evaluated and compared the protective effects of the two mouse LSC lines, YE and R5, as well as those of adult mouse hepatocyte (HC), on concanavalin A (ConA)-induced acute liver injury. YE and R5 cells were analyzed by microscopy, functional assays, and gene expression. We confirmed that YE and R5 cells were undifferentiated cells that had partial hepatocytic functions and a potential to differentiate into hepatocytes. YE cells has characteristics of LSCs at the early stage of differentiation, whereas the differentiation stage of R5 cells was later than that of YE cells. Subsequently, YE, R5, and HC cells were intraperitoneally transplanted into three groups of mice, followed by injection of ConA through the tail vein of each mouse at 12 h later. Blood tests, histology, flow cytometry, and quantitative PCR were then used to evaluate the therapeutic effects of the cell transplantations at 24 h after ConA injections. Compared with that of the ConA control group, YE, R5, and HC cells reduced the expression of alanine transaminase (ALT), aspartate aminotransferase (AST), and total bilirubin (TBIL) in serum and alleviated the degree of hepatic necrosis. Moreover, transplantation of these cells induced more regulatory T cells (Tregs) and less T-helper 17 (Th17) cells in the liver and spleen, and also promoted the expression of forkhead box protein 3 (Foxp3) and interleukin (IL)-10; in contrast, these transplantations induced various degrees of inhibition in the expression of retinoic acid-related orphan receptor γt (RORγt), IL-17A, IL-17F, and tumor necrosis factor-α (TNF-α). The protective effects of YE and R5 cells were significantly stronger than those of HC cells, and YE cells at the earlier differentiation stage than that of R5 cells exhibited the strongest protective effects. These results demonstrate that mouse LSCs at different stages of differentiation alleviate ConA-induced acute liver injury in mice by modulating Tregs, Th17 cells, and cytokine secretion.

Evidence for complete nitrification in enrichment culture of tidal sediments and diversity analysis of clade a comammox Nitrospira in natural environments.

Complete ammonia oxidizers (comammox), as novel microbial communities, are predicted to play an important role in the nitrogen cycle. Here we reported the presence of complete nitrification in tidal sediments and examined the diversity and abundance of comammox in natural ecosystems. Metagenome and metatranscriptome of the enrichment culture from tidal sediments harbored the genes of comammox. Near-complete comammox AmoA/B/C- and Hao-like sequences showed close relationships to the known comammox (with sequence identity from 79 to 99%) rather than classical betaproteobacterial ammonia-oxidizing bacteria (ß-AOB) (57 to 66%) and ammonia-oxidizing archaea (AOA) (24 to 38%). To analyze the diversity of comammox in natural environments, a new primer set targeting clade A comammox Nitrospira (COM-A) amoA genes was designed based on sequences obtained in this study and sequences from published database. In silico evaluation of the primers showed the high coverage of 89 and 100% in the COM-A amoA database. Application of the primers in six different ecosystems proved their strong availability. Community composition of COM-A suggested a relatively higher diversity than ß-AOB in similar environments. Quantification results showed that COM-A amoA genes accounted for about 0.4-5.6% in total amoA genes. These results provide novel insight into our perception of the enigmatic comammox and have significant implications for profound understanding of complex nitrification process.

Downregulation of the long non-coding RNA taurine-upregulated gene 1 inhibits glioma cell proliferation and invasion and promotes apoptosis.

Expression of the long non-coding RNA taurine-upregulated gene 1 (TUG1) is associated with various aggressive tumors. The present study aimed to investigate the biological function of TUG1 in regulating apoptosis, proliferation, invasion and cell cycle distribution in human glioma U251 cells. Lentivirus-mediated TUG1-specific microRNA was transfected into U251 cells to abrogate the expression of TUG1. Flow cytometry analysis was used to examine the cell cycle distribution and apoptosis of U251 cells. Cellular proliferation was examined using Cell Counting Kit-8 (CCK-8) assays and invasion was examined by Transwell assays. The apoptotic rate of cells in the TUG1-knockdown group was significantly higher than in the negative control (NC) group (11.58 vs. 9.14%, P<0.01). CCK-8 assay data demonstrated that the proliferative ability of cells within the TUG1-knockdown group was lower compared with that of the NC group. A Transwell invasion assay was performed, which revealed that the number of invaded cells from the TUG1-knockdown group was the less compared with that of the NC group. In addition, the G0/G1 phase population was significantly increased within the treated group (44.85 vs. 38.45%, P<0.01), as measured by flow cytometry. The present study demonstrated that the downregulation of TUG1 may inhibit proliferation and invasion, and promote glioma U251 cell apoptosis. In addition, knockdown of TUG1 may have an effect on cell cycle arrest. The data presented in the current study indicated that TUG1 may be a novel therapeutic target for glioma.

Spatial Abundance, Diversity, and Activity of Ammonia-Oxidizing Bacteria in Coastal Sediments of the Liaohe Estuary.

Ammonia-oxidizing bacteria (AOB) play an important role in nitrification in estuaries. The aim of this study was to examine the spatial abundance, diversity, and activity of AOB in coastal sediments of the Liaohe Estuary using quantitative PCR, high-throughput sequencing of the amoA gene coding the ammonia monooxygenase enzyme active subunit, and sediment slurry incubation experiments. AOB abundance ranged from 8.54 × 104 to 5.85 × 106 copies g-1 of wet sediment weight and exhibited an increasing trend from the Liaohe Estuary to the open coastal zone. Potential nitrification rates (PNRs) ranged from 0.1 to 336.8 nmol N g-1 day-1 along the estuary to the coastal zone. Log AOB abundance and PNRs were significantly positively correlated. AOB richness decreased from the estuary to the coastal zone. High-throughput sequencing analysis indicated that the majority of amoA gene sequences fell within the Nitrosomonas and Nitrosomonas-like clade, and only a few sequences were clustered within the Nitrosospira clade. This finding indicates that the Nitrosomonas-related lineage may be more adaptable to the specific conditions in this estuary than the Nitrosospira lineage. Sites with high nitrification rates were located in the southern open region and were dominated by the Nitrosomonas-like lineage, whereas the Nitrosospira lineage was found primarily in the northern estuary mouth sites with low nitrification rates. Thus, nitrification potentials in Liaohe estuarine sediments in the southern open region were greater than those in the northern estuary mouth, and the Nitrosomonas-related lineage might play a more important role than the Nitrosospira lineage in nitrification in this estuary.

SNPs in the aryl hydrocarbon receptor-interacting protein gene associated with sporadic non-functioning pituitary adenoma.

Mutations in the aryl hydrocarbon receptor-interacting protein (AIP) gene have previously been associated with a predisposition to pituitary adenomas. However, to the best of our knowledge, mutations in AIP that relate specifically to sporadic non-functioning pituitary adenomas (NFPAs) have yet to be reported. Therefore, the present study aimed to identify single nucleotide polymorphisms (SNPs) in the AIP gene that may be associated with NFPAs. Peripheral blood samples and the entire coding sequence of the AIP gene from 56 patients with NFPAs and 56 controls were analyzed in triplicate. Of the 56 patients with NFPAs, 9 patients (16.1%) were identified as harboring five different SNPs, although no germline mutations in the AIP gene were detected in any of the patients. Three different SNPs (7051C>T, 8012G>C and 8020G>C) were identified in exons 4 and 6 in 3 different patients (each in 1 patient). Two different SNPs (7318C>A and 7886A>G) were identified in exons 5 and 6, respectively, in 6 different patients (each in 3 patients). No SNPs or germline mutations in the AIP gene were identified in the controls. The results of the present study suggested that mutations in the AIP gene might not have an important role in the tumorigenesis of NFPAs. However, further studies are required in order to investigate potential molecular and genetic mechanisms that may underlie the involvement of AIP in NFPA.

[The correlation between Chlamydiae pneumonia and carotid atherosclerosis].

OBJECTIVES: To study the correlation between Chlamydiae pneumonia and carotid atherosclerosis, and the correlation between the infection of Chlamydiae pneumonia and ischemic events. METHODS: The study group consisted of 19 patients who underwent unilateral carotid endarterectomy surgery during the period from January 2010 to December 2011, and the atherosclerotic plaque specimens were harvested from these patients. The control group consisted of 10 patients who underwent extracranial-intracranial bypass surgery during the same period, and the normal external carotid artery specimens were got from these patients. The clinical data between the two groups had comparability. The presence of Chlamydiae pneumonia in atherosclerotic plaque and normal artery tissue were investigated by immunohistochemistry. The expression of Toll-like receptor 2 (TLR2), tumor necrosis factor-α (TNF-α) and vascular cell adhesion molecule-1 (VCAM-1) in the atherosclerotic plaque infected with Chlamydiae pneumonia were also detected. Data were analyzed using Fisher's exact test. RESULT: Chlamydiae pneumonia was found in 9 of 19 atherosclerotic plaques, while no positive result was found in control group. The statistical analysis showed a significant difference (P = 0.011). Among the 19 patients in study group, 15 of them had ischemic events, and Chlamydiae pneumonia was found in 9 of these 15 patients; while the other 4 patients didn't have any ischemic events and no Chlamydiae pneumonia was found in them, but there was no statistical different between them (P = 0.087). Through immunohistochemistry, the expression of Chlamydiae pneumonia, TLR2, TNF-α and VCAM-1 were found in same area. CONCLUSIONS: There is a correlation between Chlamydiae pneumonia and carotid atherosclerosis.And there might be a correlation between Chlamydiae pneumonia and cerebral ischemic events.