The characteristics of soil salinization effects on nitrogen mineralization and nitrification in upland fields

The influence of soil salinization on nitrogen (N) transformation is largely unknown, which impedes the reasonable management of N in saline fields. A comprehensive meta-analysis was thus conducted to evaluate the effects of salinity and relative soil physicochemical properties on net N mineralization and nitrification in upland soils. Results showed that effects of salinity on the net-N mineralization rate (Min) and nitrification rate (Nit) changed with the salinity level and incubation time. Generally, the inhibitory effect of salt on Min and Nit decreased gradually with incubation time. At 14–16 days of soil incubation, significant stimulatory effects on Min were observed in middle-level (ECe: 12–16 dS m-1) and high-level (ECe >16 dS m-1) saline soils, and on Nit in low-level (ECe: 4–12 dS m-1) saline soils. Regression analysis revealed that the effects of soil organic carbon (SOC), total N (TN), C/N, pH, and clay content on Min and Nit were closely related to salinity levels. Nit at 5–7 days of soil incubation first enhanced and then decreased with C/N increase, and the threshold value was 34.7. The effect of pH on Nit changed with salinity levels, and shifted from stimulation to inhibition with increasing pH. Min at 5–7 days of soil incubation in middle-level group first increased with increasing pH, and decreased when pH was higher than 8.1. Salinization deeply affected soil properties, which further influenced N turnover via alteration of the availability of substrates and microbial biomass and activities. Our findings suggest that the influence of salinity on soil N turnover closely related with salinity level, and salinity level should be considered fully when optimizing N management in saline upland fields

Targeted Next Generation Sequencing Revealed a Novel Homozygous Loss-of-Function Mutation in ILDR1 Gene Causes Autosomal Recessive Nonsyndromic Sensorineural Hearing Loss in a Chinese Family

Hereditary hearing impairment is one of the major and common birth defects in Chinese population. Non-syndromic sensorineural hearing loss (NSHL) is the most common types of hereditary hearing impairment. Genotypically and phenotypically NSHL is extremely heterogenous and follow either autosomal dominant or autosomal recessive or X-linked mode of inheritance. Presently, 127 genes have been identified to be associated with both syndromic and (NSHL). Here, we studied a Chinese family with moderate and profound hearing impairment. The proband is a 30-year old Chinese man. The proband was born with normal hearing and at the age of 5-years, the proband was first noticed with hearing impairment. Gradually and progressively the proband was presented with loss of hearing in his both right and left ears at the age of 30 years. The clinical symptoms, age of onset or progression to loss of hearing was similar in both the proband and his younger brother. The proband’s parents are phenotypically normal and non-consanguineous. Clinical diagnosis of the proband and his younger brother has been done by classical pure tone audiogram (PTA). Computed Tomography (CT) found no abnormality in bilateral external ear, middle ear and inner ear. Targeted next generation sequencing was performed with a panel of 127 genes reported to be associated with hereditary hearing impairment. A novel homozygous single nucleotide deletion (c.427delT) in exon 4 of ILDR1 gene has been identified in proband and in his younger brother. Sanger sequencing confirmed that proband’s father and mother are carrying this mutation in a heterozygous manner. This mutation has not been identified in 100 normal healthy control individuals. This mutation (c.427delT) causes frameshift (p.Tyr143Ilefs∗19) which leads to the formation of a truncated ILDR1 protein of 162 amino acids instead of the wild type ILDR1 protein of 546 amino acids. ILDR1 associated hereditary hearing impairment is very rare and this is the first report of identifying a loss-of-function mutation in ILDR1 gene associated with hereditary hearing impairment in Chinese population. Our present study also emphasized the significance of rapid, accurate and cost-effective screening for the patient with hereditary hearing impairment by targeted next generation sequencing

COPB2 gene silencing inhibits colorectal cancer cell proliferation and induces apoptosis via the JNK/c-Jun signaling pathway.

ObjectivesColorectal cancer (CRC) is one of the most common malignant human tumors. It is associated with high morbidity and mortality rates. In recent years, tumor gene therapy has emerged as a promising new approach for colorectal cancer therapy. Herein, we identify and analyze the role of COPB2 (coatomer protein complex, subunit beta 2) in proliferation and apoptosis of CRC cells.MethodsTo investigate the role of COPB2 in the proliferation and apoptosis of CRC cells, a shCOPB2 vector and a shCtrl vector were constructed for transfection into RKO and HCT116 cells. Cells proliferation was subsequently measured via cell counting kit-8 (CCK8) assay and Celigo cell counting assay. Apoptosis was measured via flow cytometry. The activity level of Caspase 3/7 was measured. Finally, the level of several JNK/c-Jun apoptosis pathway-related proteins were measured to characterize the mechanism of apoptosis.ResultsOur results showed that the proliferation rate was decreased and the apoptosis rate was increased in shCOPB2-treated RKO and HCT116 cells compared to those in controls. After the silencing of COPB2, JNK/c-Jun signal pathway activation was increased, the expression levels of apoptosis pathway-related proteins, such as Bad, p53 and Caspase 3, were also increased.ConclusionCOPB2 gene silencing can inhibit RKO and HCT116 cells proliferation and induce apoptosis via the JNK/c-Jun signaling pathway

Silencing of NLRP3 Sensitizes Chemoresistant Ovarian Cancer Cells to Cisplatin

Background. Ovarian cancer is a fatal gynecological malignancy. The resistance to chemotherapy in ovarian cancer treatment has been a thorny issue. This study is aimed at probing the molecular mechanism of cisplatin (DDP) resistance in ovarian cancer. Methods. Bioinformatics analysis was conducted to examine the role of Nod-like receptor protein 3 (NLRP3) in ovarian cancer. The NLRP3 level in DDP-resistant ovarian cancer tumors and cell lines (SKOV3/DDP and A2780/DDP) was evaluated by applying immunohistochemical staining, western blot, and qRT-PCR. Cell transfection was conducted to regulate the NLRP3 level. Cell abilities to proliferate, migrate, invade, and apoptosis were measured employing colony formation, CCK-8, wound healing, transwell, and TUNEL assays, respectively. Cell cycle analysis was completed via flow cytometry. Corresponding protein expression was measured by western blot. Results. NLRP3 was overexpressed in ovarian cancer, correlated with poor survival, and upregulated in DDP-resistant ovarian cancer tumors and cells. NLRP3 silencing exerted antiproliferative, antimigrative, anti-invasive, and proapoptotic effects in A2780/DDP and SKOV3/DDP cells. Additionally, NLRP3 silencing inactivated NLRPL3 inflammasome and blocked epithelial-mesenchymal transition via enhancing E-cadherin and lowering vimentin, N-cadherin, and fibronectin. Conclusion. NLRP3 was overexpressed in DDP-resistant ovarian cancer. NLRP3 knockdown hindered the malignant process of DDP-resistant ovarian cancer cells, providing a potential target for DPP-based ovarian cancer chemotherapy

Cloning and Expression Analysis of Vvlcc3, a Novel and Functional Laccase Gene Possibly Involved in Stipe Elongation

Volvariella volvacea, usually harvested in its egg stage, is one of the most popular mushrooms in Asia. The rapid transition from the egg stage to elongation stage, during which the stipe stretches to almost full length leads to the opening of the cap and rupture of the universal veil, and is considered to be one of the main factors that negatively impacts the yield and value of V. volvacea. Stipe elongation is a common phenomenon in mushrooms; however, the mechanisms, genes and regulation involved in stipe elongation are still poorly understood. In order to study the genes related to the stipe elongation, we analyzed the transcription of laccase genes in stipe tissue of V. volvacea, as some laccases have been suggested to be involved in stipe elongation in Flammulina velutipes. Based on transcription patterns, the expression of Vvlcc3 was found to be the highest among the 11 laccase genes. Moreover, phylogenetic analysis showed that VvLCC3 has a high degree of identity with other basidiomycete laccases. Therefore, we selected and cloned a laccase gene, named Vvlcc3, a cDNA from V. volvacea, and expressed the cDNA in Pichia pastoris. The presence of the laccase signature L1-L4 on the deduced protein sequence indicates that the gene encodes a laccase. Phylogenetic analysis showed that VvLCC3 clusters with Coprinopsis cinerea laccases. The ability to catalyze ABTS (2,2’-Azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) oxidation proved that the product of the Vvlcc3 gene was a functional laccase. We also found that the expression of the Vvlcc3 gene in V. volvacea increased during button stage to the elongation stage; it reached its peak in the elongation stage, and then decreased in the maturation stage, which was similar to the trend in the expression of Fv-lac3 and Fv-lac5 in F. velutipes stipe tissue. The similar trend in expression level of these laccase genes of F. velutipes suggested that this gene could be involved in stipe elongation in V. volvacea

Agricultural reclamation effects on ecosystem CO2 exchange of a coastal wetland in the Yellow River Delta

Little is known about the impacts of agricultural exploitation of coastal wetlands on ecosystem CO2 exchange, although coastal wetlands have been widely reclaimed for agricultural use across the world. We measured net ecosystem CO2 exchange (NEE) and its major components, gross primary production (GPP) and ecosystem respiration (R-eco) using an eddy covariance flux technique in a natural coastal wetland (reed) and an adjacent, newly reclaimed farmland (cotton) in the Yellow River Delta, China. The results showed that agricultural reclamation changed the ecosystem CO2 exchange of the coastal wetland at three distinct levels. Initially, the conversion from the wetland to farmland changed the light response parameters (alpha, A(max), and R-eco, day) of NEE and temperature sensitivity (Q(10)) of R-eco mainly by changing the dominant vegetation type. Over the growing season, NEE, R-eco and GPP were significantly correlated with LAI at both sites and aboveground biomass at the farmland site. Next, the reclamation of wetland modified the diurnal and seasonal dynamics of ecosystem CO2 exchange. Significant differences in diurnal variations of NEE between the wetland and farmland sites were found during the growing season (with the exception of June and July). Seasonal means of daily GPP and R-eco values at the wetland site were higher than those at the farmland. Ultimately, the agricultural reclamation altered the CO2 sequestration capacity of the coastal wetland. The cumulative NEE in the wetland (-237.4 g Cm-2) was higher than that in the farmland (-202.0 g Cm-2). When biomass removal was taken into account, the farmland was a strong source for CO2 of around 131.9 g Cm-2 during the growing season. Overall, land use changes by reclamation altered ecosystem CO2 exchange at several ecological scales by changing the dominant vegetation type and altering the ecosystem's natural development. (C) 2013 Elsevier B.V. All rights reserved.Little is known about the impacts of agricultural exploitation of coastal wetlands on ecosystem CO2 exchange, although coastal wetlands have been widely reclaimed for agricultural use across the world. We measured net ecosystem CO2 exchange (NEE) and its major components, gross primary production (GPP) and ecosystem respiration (R-eco) using an eddy covariance flux technique in a natural coastal wetland (reed) and an adjacent, newly reclaimed farmland (cotton) in the Yellow River Delta, China. The results showed that agricultural reclamation changed the ecosystem CO2 exchange of the coastal wetland at three distinct levels. Initially, the conversion from the wetland to farmland changed the light response parameters (alpha, A(max), and R-eco, day) of NEE and temperature sensitivity (Q(10)) of R-eco mainly by changing the dominant vegetation type. Over the growing season, NEE, R-eco and GPP were significantly correlated with LAI at both sites and aboveground biomass at the farmland site. Next, the reclamation of wetland modified the diurnal and seasonal dynamics of ecosystem CO2 exchange. Significant differences in diurnal variations of NEE between the wetland and farmland sites were found during the growing season (with the exception of June and July). Seasonal means of daily GPP and R-eco values at the wetland site were higher than those at the farmland. Ultimately, the agricultural reclamation altered the CO2 sequestration capacity of the coastal wetland. The cumulative NEE in the wetland (-237.4 g Cm-2) was higher than that in the farmland (-202.0 g Cm-2). When biomass removal was taken into account, the farmland was a strong source for CO2 of around 131.9 g Cm-2 during the growing season. Overall, land use changes by reclamation altered ecosystem CO2 exchange at several ecological scales by changing the dominant vegetation type and altering the ecosystem's natural development. (C) 2013 Elsevier B.V. All rights reserved