Role of phosphate in microalgal-bacterial symbiosis system treating wastewater containing heavy metals.

Phosphorus is one of the important factors to successfully establish the microalgal-bacterial symbiosis (MABS) system. The migration and transformation of phosphorus can occur in various ways, and the effects of phosphate on the MABS system facing environmental impacts like heavy metal stress are often ignored. This study investigated the roles of phosphate on the response of the MABS system to zinc ion (Zn2+). The results showed that the pollutant removal effect in the MABS system was significantly reduced, and microbial growth and activity were inhibited with the presence of Zn2+. When phosphate and Zn2+ coexisted, the inhibition effects of pollutants removal and microbial growth rate were mitigated compared to that of only with the presence of Zn2+, with the increasing rates of 28.3% for total nitrogen removal, 48.9% for chemical oxygen demand removal, 78.3% for chlorophyll-a concentration, and 13.3% for volatile suspended solids concentration. When phosphate was subsequently supplemented in the MABS system after adding Zn2+, both pollutants removal efficiency and microbial growth and activity were not recovered. Thus, the inhibition effect of Zn2+ on the MABS system was irreversible. Further analysis showed that Zn2+ preferentially combined with phosphate could form chemical precipitate, which reduced the fixation of MABS system for Zn2+ through extracellular adsorption and intracellular uptake. Under Zn2+ stress, the succession of microbial communities occurred, and Parachlorella was more tolerant to Zn2+. This study revealed the comprehensive response mechanism of the co-effects of phosphate and Zn2+ on the MABS system, and provided some insights for the MABS system treating wastewater containing heavy metals, as well as migration and transformation of heavy metals in aquatic ecosystems.

Revealing mechanisms of triclosan on the removal and distribution of nitrogen and phosphorus in microalgal-bacterial symbiosis system.

Microalgal-bacterial symbiosis (MABS) system performs synergistic effect on the reduction of nutrients and carbon emissions in the water treatment process. However, antimicrobial agents are frequently detected in water, which influence the performance of MABS system. In this study, triclosan (TCS) was selected to reveal the effects and mechanisms of antimicrobial agents on MABS system. Results showed that the removal efficiencies of chemical oxygen demand, NH4+-N and total phosphorus decreased by 3.0%, 24.0% and 14.3% under TCS stress. In contrast, there were no significant decrease on the removal effect of total nitrogen. Mechanism analysis showed that both the growth rate of microorganisms and the nutrients retention capacity of extracellular polymeric substances were decreased. The intracellular accumulation for nitrogen and phosphorus was promoted due to the increased cytomembrane permeability caused by lipid peroxidation. Moreover, microalgae were dominant in MABS system with ratio between microalgae and bacteria of more than 5.49. The main genus was Parachlorella, with abundance of more than 90%. Parachlorella was highly tolerant to TCS, which might be conductive to maintain its survival. This study revealed the nutrients pathways of MABS system under TCS stress, and helped to optimize the operation of MABS system.

The expression of CD86 in CD3+CD56+ NKT cells is associated with the occurrence and prognosis of sepsis-associated encephalopathy in sepsis patients: a prospective observational cohort study.

The role of CD3+CD56+ natural killer T (NKT) cells and its co-signaling molecules in patients with sepsis-associated encephalopathy (SAE) is unknown. In this prospective observational cohort study, we initially recruited 260 septic patients and eventually analyzed 90 patients, of whom 57 were in the SAE group and 37 were in the non-SAE group. Compared to the non-SAE group, 28-day mortality was significantly increased in the SAE group (33.3% vs. 12.1%, p = 0.026), while the mean fluorescence intensity (MFI) of CD86 in CD3+CD56+ NKT cells was significantly lower (2065.8 (1625.5 ~ 3198.8) vs. 3117.8 (2278.1 ~ 5349), p = 0.007). Multivariate analysis showed that MFI of CD86 in NKT cells, APACHE II score, and serum albumin were independent risk factors for SAE. Furthermore, the Kaplan-Meier survival analysis indicated that the mortality rate was significantly higher in the high-risk group than in the low-risk group (χ2 = 14.779, p < 0.001). This study showed that the decreased expression of CD86 in CD3+CD56+ NKT cells is an independent risk factor of SAE; thus, a prediction model including MFI of CD86 in NKT cells, APACHE II score, and serum albumin can be constructed for diagnosing SAE and predicting prognosis.

Pcv-aCO2 and procalcitonin levels for the early diagnosis of bloodstream infections caused by gram-negative bacteria.

BACKGROUND: The central venous-to-arterial carbon dioxide difference (Pcv-aCO2) is a biomarker for tissue perfusion, but the diagnostic value of Pcv-aCO2 in bacteria bloodstream infections (BSI) caused by gram-negative (GN) bacteria remains unclear. This study evaluated the expression levels and diagnostic value of Pcv-aCO2 and procalcitonin (PCT) in the early stages of GN bacteria BSI. METHODS: Patients with BSI admitted to the intensive care unit at Guangdong Provincial People's Hospital between August 2014 and August 2017 were enrolled. Pcv-aCO2 and PCT levels were evaluated in GN and gram-positive (GP) bacteria BSI patients. RESULTS: A total of 132 patients with BSI were enrolled. The Pcv-aCO2 (8.32 ± 3.59 vs 4.35 ± 2.24 mmHg p = 0.001) and PCT (30.62 ± 34.51 vs 4.92 ± 6.13 ng/ml p = 0.001) levels were significantly higher in the GN group than in the GP group. In the diagnosis of GN bacteria BSI, the area under the receiver operating characteristic curve (AUROC) for Pcv-aCO2 was 0.823 (95% confidence interval (CI): 0.746-0.900). The sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) were 71.90%, 88.00%, 74.07% and 78.21%, respectively. The AUROC for PCT was 0.818 (95% CI: 0.745-0.890). The sensitivity, specificity, PPV and NPV were 57.90%, 94.67%, 71.93% and 74.67%, respectively. CONCLUSIONS: Pcv-aCO2 and PCT have similar and high diagnostic value for the early diagnosis of BSI caused by GN bacteria.

Exosome-Derived lncRNA NEAT1 Exacerbates Sepsis-Associated Encephalopathy by Promoting Ferroptosis Through Regulating miR-9-5p/TFRC and GOT1 Axis.

Sepsis can cause sepsis-associated encephalopathy (SAE), but whether SAE was induced or exacerbated by ferroptosis remains unknown. In this study, the rat sepsis model was constructed using the cecal ligation and puncture method. The blood-brain barrier (BBB) permeability was measured by Evans blue dye (EBD) in vivo. The levels of ROS, Fe ion, MDA, GSH, and GPX4 were assessed by enzyme-linked immunosorbent assay (ELISA). The exosomes isolated from serum were cultured with bEnd.3 cells for the in vitro analysis. Moreover, bEnd.3 cells cultured with 100 µM FeCl3 (iron-rich) were to simulate ferroptosis stress. The cell viability was evaluated by Cell Counting Kit-8 (CCK-8) assay. A dual-luciferase reporter gene assay was performed to confirm the relationship between miR-9-5p with NEAT1, TFRC, and GOT1. In vivo, it is found that BBB permeability was damaged in model rats. Level of ROS, Fe ion, and MDA was increased, and level of GSH and GPX4 was decreased, which means ferroptosis was induced by sepsis. Exosome-packaged NEAT1 in serum was significantly upregulated in model rats. In vitro, it is found that NEAT1 functions as a ceRNA for miR-9-5p to facilitate TFRC and GOT1 expression. Overexpression of NEAT1 enhanced ferroptosis stress in bEnd.3 cells. Increased miR-9-5p alleviated sepsis-induced ferroptosis by suppressing the expression of TFRC and GOT1 both in vivo and in vitro. In conclusion, these findings suggest that sepsis induced high expression of serous exosome-derived NEAT1, and it might exacerbate SAE by promoting ferroptosis through regulating miR-9-5p/TFRC and GOT1 axis.

[Effects of P fertilizer on female strobilus and needle N and P nutrition of Pinus massoniana clones with different fruiting abilities.] / ç£·è‚¥å¯¹ä¸åŒç»“å®žèƒ½åŠ›é©¬å°¾æ¾æ— æ€§ç³»é›ŒçƒèŠ±é‡åŠé’ˆå¶æ°®ç£·è¥å »çš„å½±å“.

In order to realize precise fertilization and high yield management of Pinus massoniana clonal seed orchard, clones with different fruiting abilities were used as the materials. Four P fertilization levels were at 0, 400, 800 and 1600 g per plant (P0, P4, P8 and P16 respectively). Fertilization was applied before floral primordia formation and after cone picked, respectively. The effects of P fertilizer on the female strobilus of P. massoniana clones and the changes of N, P contents in needles of different positions during floral primordia formation stage and early stage of flower bud differentiation were investigated. The results showed that compared with P0, the female strobilus of P8 and P16 were significantly increased by 67.4% and 61.2% in 2018 and 28.9% and 14.1% in 2019, respectively. There was a significant negative correlation between the female strobilus with the N content and N/P, a significant positive correlation between the female strobilus and the P content in needles. The responses of N and P contents in needles to P fertilization differed in clones with different fruiting abilities. In floral primordia formation stage, the N content of clones with weak fruiting ability was high, and the N/P was 11.5-12.5, while the P content of clones with strong fruiting abilities was high, and the N/P was 9.5-10.5. During this period, the P content of most clones under P8 treatment was the highest, while the N/P was lowest. In the early stage of flower bud differentiation, the N/P of two fruiting clones was 15.3-17.0 and 13.2-15.1, respectively. The P content in upside layer was significantly higher while N/P was significantly lower than that in middle and lower layers. In conclusion, the 800 g P fertilization per plant could increase the P content and reduce the N/P of needles during the floral primordia formation stage of clones with diffe-rent fruiting abilities, which was beneficial to the formation of female strobilus and promote the yield of clone seed orchards.

JAK/STAT signaling pathway-mediated microRNA-181b promoted blood-brain barrier impairment by targeting sphingosine-1-phosphate receptor 1 in septic rats.

BACKGROUND: Blood-brain barrier (BBB) impairment plays a significant role in the pathogenesis of sepsis-associated encephalopathy (SAE). However, the molecular mechanisms are poorly understood. In the present study, we aimed to investigate the regulatory relationship between the Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling pathway, microRNA (miR)-181b and its target genes in sepsis in vivo and in vitro. METHODS: Four rat models (sham, sepsis, sepsis plus STAT3 inhibitor (Stattic), and sepsis plus miR-181b inhibitor [sepsis + anta-miR-181b]) were established. For the in vitro experiments, rat brain microvascular endothelial cells (rBMECs) and rat brain astrocytes (rAstrocytes) were cultured with 10% serum harvested from sham, sepsis, and sepsis + anta-miR-181b rats. Chromatin immunoprecipitation-quantitative polymerase chain reaction (ChIP-QPCR) analysis was carried out to detect the binding and enrichment of the JAK/STAT3 signal core transcription complex in the miR-181b promoter region. Dual-luciferase reporter gene assay was conducted to test miR-181b and its target genes. The cell adhesion rate of rBMECs was also measured. RESULTS: During our investigations, the expression levels of miR-181b, p-JAK2, p-STAT3, and C/EBPß were found to be significantly increased in the septic rats compared with the sham rats. STAT3 inhibitor halted BBB damage by downregulating the expression of miR-181b. In addition, miR-181b targeted sphingosine-1-phosphate receptor 1 (S1PR1) and neurocalcin delta (NCALD). The up-regulated miR-181b significantly decreased the cell adhesion rate of rBMECs. The administration of miR-181b inhibitor reduced damage to the BBB through increasing the expression of S1PR1 and NCALD, which again proved that miR-181b negatively regulates SIPR1 and NCALD to induce BBB damage. CONCLUSIONS: Our study demonstrated that JAK2/STAT3 signaling pathway induced expression of miR-181b, which promoted BBB impairment in rats with sepsis by downregulating S1PR1 and decreasing BBB cell adhesion. These findings strongly suggest JAK2/STAT3/miR-181b axis as therapeutic target in protecting against sepsis-induced BBB damage.

Patterns of Deterioration in Moderate Patients With COVID-19 From Jan 2020 to Mar 2020: A Multi-Center, Retrospective Cohort Study in China.

Background: Around the globe, moderate cases account for the largest proportion of all coronavirus disease 2019 (COVID-19) patients, and deteriorated moderate patients contribute the most in mortality. However, published articles failed to address the deterioration details of moderate cases, especially on when and how they deteriorated. Methods: All moderate COVID-19 patients hospitalized in Guangdong Province from January 14 to March 16, 2020, were included in this multicenter retrospective cohort study and were divided into deteriorated and non-deteriorated groups according to clinical status. Symptoms and demographic, therapeutic, and laboratory test result characteristics were collected to explore the features of disease deterioration. Results: Of 1,168 moderate patients included, 148 (13%) deteriorated to severe (130 cases) or critical (18 cases) status. Over 20% of the older subgroup (>50 years old) showed deterioration. The median time for deterioration was 11 days after onset [interquartile range (IQR) 9-14 days]. In addition, 12.2% severe cases could further develop to critical status after 3 days (IQR 2-6.5 days) of having a severe condition. Respiratory dysfunction and hypoxia were the major manifestations as disease deterioration, while 76 cases (52.1%) showed respiratory rate >30 breaths/min, 119 cases (80.4%) showed SaO2 <93%, 100 cases (67.5%) had 201 < PaO2/FiO2 < 300, and 27 cases (18.9%) had blood lactic acid >2.0 mmol/L. In view of multiple organ dysfunction, 87.8% of acute respiratory distress syndrome (ARDS), 20.2% of acute kidney injury (AKI), 6.8% of coagulopathy, 4% of acute heart failure (AHF), 3.4% of acute hepatic injury (AHI), and 5.4% of shock occurred in deteriorated patients, while organ injury occurred in the following sequence: ARDS, AKI, AHF, coagulopathy, AHI, and shock. Conclusions: The deteriorated pattern of moderate COVID-19 patients is characterized as the 11th day from onset (IQR 9-14 days) being an important time point of disease deterioration with further exacerbation to critical condition in 3 days (IQR 2-6.5 days), A RDS followed by AKI being the typical modes of sequential organ damage.

Epidemiological and Clinical Findings of Short-Term Recurrence of Severe Acute Respiratory Syndrome Coronavirus 2 Ribonucleic Acid Polymerase Chain Reaction Positivity in 1282 Discharged Coronavirus Disease 2019 Cases: A Multicenter, Retrospective, Observational Study.

BACKGROUND: Short-term recurrence of positive severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) ribonucleic acid (RNA) polymerase chain reaction (PCR) in discharged coronavirus disease 2019 (COVID-19) patients attracts the public's concern. This study aimed to determine the clinical and epidemiological results of such patients. METHODS: This retrospective study was conducted on 32 designated hospitals for COVID-19 patients discharged from January 14 to March 10, 2020. After 28-day followed-up, patients who tested positive again for SARS-CoV-2 RNA and confirmed by reverse-transcriptase polymerase chain reaction were re-admitted to hospital for further treatments. All of the close contacts of patients who tested positive again were asked to self-segregate for 14 days. Data of epidemiology, symptoms, laboratory tests, and treatments were analyzed in those patients, and their close contacts were investigated. RESULTS: Of 1282 discharged patients, 189 (14.74%) tested positive again for SARS-CoV-2 RNA during 28-day follow-up. The median time from discharge to the next positive test was 8 days (interquartile range [IQR], 5-13). Patients in the group that tested positive again were younger (34 vs 45 years, P < .001) with a higher proportion of moderate symptoms (95.77% vs 84.35%, P < .001) in the first hospitalization than in the negative group. During the second hospitalization, all patients who tested positive again showed normal peripheral white blood cells and lymphocytes and no new symptoms of COVID-19; 78.31% further improved on chest computed tomography scan compared with the first discharge, yet 25.93% accepted antiviral therapy. The median time of re-positive to negative test was 8 days (IQR, 4-15). None of the close contacts developed COVID-19. CONCLUSIONS: Our data suggest that the short-term recurrence of positive SARS-CoV-2 RNA in discharged patients is not a relapse of COVID-19, and the risk of onward transmission is very low. This provides important information for managing COVID-19 patients.

Effects of dexmedetomidine on heart rate control and pre-operative outcome in patients with acute aortic dissection: a propensity-matched analysis.

BACKGROUND: The total survival rate in patients with acute aortic dissection (AAD) has been greatly improved because of surgical technique advances. However, the pre-operative mortality rate remained high. In this study, we sought to evaluate the effects of dexmedetomidine (DEX) on heart rate control and preoperative outcome in AAD. METHODS: Retrospectively enrolled 461 patients who were diagnosed with AAD during the first 7-day after admission and divided into two groups according to the use of intravenous DEX: DEX group (91 patients) and Control group (370 patients). The heart rate and systolic blood pressure (SBP) level in both groups were recorded, and the incidence of aortic dissection rupture and pre-operative survival rates within 7 days were considered as the primary clinical outcomes. RESULTS: Compared to the Control group, heart rate of DEX group in the early 3 hours was significantly higher (P=0.009), and the 24-hour heart rate fluctuation was smaller (P=0.012). There was no difference in the systolic blood pressure (SBP) between the two groups, but the 24-hour fluctuation of SBP in DEX group was less (P=0.003). We performed a propensity-matched analysis to minimize selection bias and found that there were 7 (7.9%) patients in the DEX group occurred acute pulmonary edema, 17 (19.1%) patients in the Control group (P=0.047). And the pre-operative survival rates within 7 days were significantly improved in DEX group (P=0.004). And the pre-operative survival rates within 7 days were significantly improved in DEX group (P=0.004). CONCLUSIONS: DEX can be beneficial to facilitate heart rate control, keep SBP more steady, and reduce the incidence of pre-operative aortic rupture in patients with AAD.

Hypertonic saline mediates the NLRP3/IL-1ß signaling axis in microglia to alleviate ischemic blood-brain barrier permeability by downregulating astrocyte-derived VEGF in rats.

INTRODUCTION: The aim of this study was to explore whether the antibrain edema of hypertonic saline (HS) is associated with alleviating ischemic blood-brain barrier (BBB) permeability by downregulating astrocyte-derived vascular endothelial growth factor (VEGF), which is mediated by microglia-derived NOD-like receptor protein 3 (NLRP3) inflammasome. METHODS: The infarct volume and BBB permeability were detected. The protein expression level of VEGF in astrocytes in a transient focal brain ischemia model of rats was evaluated after 10% HS treatment. Changes in the NLRP3 inflammasome, IL-1ß protein expression, and the interleukin-1 receptor (IL1R1)/pNF-кBp65/VEGF signaling pathway were determined in astrocytes. RESULTS: HS alleviated the BBB permeability, reduced the infarct volume, and downregulated the expression of VEGF in astrocytes. HS downregulates IL-1ß expression by inhibiting the activation of the NLRP3 inflammasome in microglia and then downregulates VEGF expression by inhibiting the phosphorylation of NF-кBp65 mediated by IL-1ß in astrocytes. CONCLUSIONS: HS alleviated the BBB permeability, reduced the infarct volume, and downregulated the expression of VEGF in astrocytes. HS downregulated IL-1ß expression via inhibiting the activation of the NLRP3 inflammasome in microglia and then downregulated VEGF expression through inhibiting the phosphorylation of NF-кBp65 mediated by IL-1ß in astrocytes.

Hypertonic saline protects brain endothelial cells against hypoxia correlated to the levels of epidermal growth factor receptor and interleukin-1ß.

OBJECTIVE: The aim of this study was to verify the protective effect of hypertonic saline (HS) on brain endothelial cells under hypoxic conditions and the relevant underlying mechanism. METHODS: bEnd.3 cells were treated with oxygen-glucose deprivation (OGD)-induced injury. To measure HS performance, cell viability was determined using the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium salt assay, and cell apoptosis was assessed by flow cytometry and Terminal deoxynucleotidyl transferase UTP nick-end labeling staining. RNA-seq was performed to assess the expression profiles and screen the candidate genes that participated in OGD-induced injury and the HS protective effect. Quantitative real-time polymerase chain reaction (qPCR) and western blot analysis were used to confirm the expression of candidate genes, and enzyme-linked immunosorbent assay was used to measure the level of interleukin (IL)-1ß. Overexpression analyses were performed to confirm the functions of the differentially expressed genes. RESULTS: HS with a concentration of 40 mmol/L NaCl had an obvious protective effect on bEnd.3 cells after OGD-induced injury, resulting in increased cell viability and a smaller percentage of apoptotic cells. According to the RNA-seq results, epidermal growth factor receptor (EGFR) was chosen as the differentially expressed gene target in this study. The qPCR and western blot analyses further confirmed that the levels of EGFR/phosphorylated epidermal growth factor receptor and IL-1ß were enhanced after OGD-induced injury, but attenuated after treatment with 40 mmol/L of NaCl HS. Overexpressed EGFR reversed the protective effect of HS that caused low viability and high rates of apoptosis in cells. CONCLUSION: HS can protect endothelial cells against OGD-induced injury, but is affected by the expression of EGFR/p-EGFR and IL-1ß.

[Priming Effects of Soil Moisture on Soil Respiration Under Different Tillage Practices].

In the early stage of an incubation experiment, soil respiration has a sensitive response to different levels of soil moisture. To investigate the effects of soil moisture on soil respiration under different tillage practices, we designed an incubation trial using air-dried soil samples collected from tillage experiment station established on black soils in 2001. The tillage experiment consisted of no-tillage (NT), ridge tillage (RT), and conventional tillage (CT). According to field capacity (water-holding capacity, WHC), we set nine moisture levels including 30%, 60%, 90%, 120%, 150%, 180%, 210%, 240%, 270% WHC. During the 22-day short-term incubation, soil CO2 emission was measured. In the early stage of incubation, the priming effects occurred under all tillage practices. There were positive correlations between soil respiration and soil moisture. In addition to drought and flood conditions, soil CO2 fluxes followed the order of NT > RT > CT. We fitted the relationship between soil moisture and soil CO2 fluxes under different tillage practices. In the range of 30%-270% WHC, soil CO2 fluxes and soil moisture fitted a quadratic regression equation under NT, and linear regression equations under RT and CT. Under the conditions of 30%-210% WHC of both NT and RT, soil CO2 fluxes and soil moisture were well fitted by the logarithmic equation with fitting coefficient R² = 0.966 and 0.956, respectively.

[Effects of corn and soybean straws returning on CO2 efflux at initial stage in black soil].

In this study, the CO2 emission characteristics and its relationships with C and N concentration in soil amended with different types of residues were studied by thermostatic incubation method to investigate the decomposition characteristics of different types of residues after adding to the soil and the effect of C, N concentration in residues on carbon sequestration. The results showed that during 61 days incubation, the CO2 efflux rates in the soils added with the different residues changed over time and exhibited an initial decrease, followed by a stable low plateau, and then an increase to a high plateau and finally followed by a decrease. The characteristics of CO2 emissions varied with residues, with the differences mainly occurring in the starting and duration of the high plateau CO2 emission period. The cumulative CO2-C emission was significantly affected by residue type. The cumulative CO2-C emissions from soils amended with corn roots, bottom corn stalks, corn leaves, and soybean leaves (about 160 µmol · g(-1) of soil and residue) were significantly greater than those from soils amended with other residues for the initial 21 days. Except for soybean leaves, the cumulative soil CO2 emissions over the 61 day incubation period from soils amended with soybean residues were higher than that from soil amended with corn residues. There were significant linear relationships between the ratio of cumulative CO2-C emission to residue carbon concentration (CR), and both C/N and nitrogen concentration of residues in the initial 21 days incubation, but not for the entire 61 days incubation. Our study suggested that soil CO2 emission was closely dependent upon the type of residue. Soybean residues decomposed more easily than corn residues. However, the decay rate of soybean residues was slower than that of corn residues at the initial stage of incubation. Soil CO2 emission was significantly affected by the C/N ratios and nitrogen concentrations of crop residues only at the early phase of incubation.

[Effects of Different Residue Part Inputs of Corn Straws on CO2 Efflux and Microbial Biomass in Clay Loam and Sandy Loam Black Soils].

The decomposed rate of crop residues is a major determinant for carbon balance and nutrient cycling in agroecosystem. In this study, a constant temperature incubation study was conducted to evaluate CO2 emission and microbial biomass based on four different parts of corn straw (roots, lower stem, upper stem and leaves) and two soils with different textures (sandy loam and clay loam) from the black soil region. The relationships between soil CO2 emission, microbial biomass and the ratio of carbon (C) to nitrogen (N) and lignin of corn residues were analyzed by the linear regression. Results showed that the production of CO2 was increased with the addition of different parts of corn straw to soil, with the value of priming effect (PE) ranged from 215. 53 µmol . g-1 to 335. 17 µmol . g -1. Except for corn leaves, the cumulative CO2 production and PE of clay loam soil were significantly higher than those in sandy loam soil. The correlation of PE with lignin/N was obviously more significant than that with lignin concentration, nitrogen concentration and C/N of corn residue. The addition of corn straw to soil increased the contents of MBC and MBN and decreased MBC/MBN, which suggested that more nitrogen rather than carbon was conserved in microbial community. The augmenter of microbial biomass in sandy loam soil was greater than that in clay loam soil, but the total dissolved nitrogen was lower. Our results indicated that the differences in CO2 emission with the addition of residues to soils were primarily ascribe to the different lignin/N ratio in different corn parts; and the corn residues added into the sandy loam soil could enhance carbon sequestration, microbial biomass and nitrogen holding ability relative to clay loam soil.

[Impact of tillage practices on microbial biomass carbon in top layer of black soils].

A study was conducted on a long-term (13 years) tillage and rotation experiment on black soil in northeast China to determine the effects of tillage, time and soil depth on soil microbial biomass carbon (MBC). Tillage systems included no tillage (NT), ridge tillage (RT) and mould-board plough (MP). Soil sampling was done at 0-5, 5-10 and 10-20 cm depths in June, August and September, 2013, and April, 2014 in the corn phase of corn-soybean rotation plots. MBC content was measured by the chloroform fumigation extraction (CFE) method. The results showed that the MBC content varied with sampling time and soil depth. Soil MBC content was the lowest in April for all three tillage systems, and was highest in June for MP, and highest in August for NT and RT. At each sampling time, tillage system had a significant effect on soil MBC content only in the top 0-5 cm layer. The MBC content showed obvious stratification under NT and RT with a higher MBC content in the top 0-5 cm layer than under MP. The stratification ratios under NT and RT were greatest in September when they were respectively 67.8% and 95.5% greater than under MP. Our results showed that soil MBC contents were greatly affected by the time and soil depth, and were more apparently accumulated in the top layer under NT and RT.

Acute myocardial ischemia directly modulates the expression of brain natriuretic peptide at the transcriptional and translational levels via inflammatory cytokines.

Cardiomyocyte stretching has been reported to be a major trigger for brain natriuretic peptide (BNP) release; however, an increase in circulating BNP is observed in patients with acute myocardial ischemia in the absence of increased left ventricular wall stress or cardiomyocyte stretching. In the present study, to investigate the direct and independent effects of acute myocardial ischemia on BNP expression and its mechanism, we established an in vitro glucose-free ischemia and hypoxia injured model of cultured rat cardiomyotes and proved hypoxia upregulated expressions of interleukin-6(il-6) and BNP. Further treatment with il-6 elicited dose- and time-dependent increases in BNP mRNA and protein expression as well as an upregulation in transforming growth factor-ß1 (TGF-ß1)/Smad2 expression, which was partially suppressed by a neutralizing antibody. In conclusion, our study showed that acute myocardial ischemia can directly upregulate BNP expression at the translational and transcriptional levels through the action of il-6, and this process is associated with the upregulation of TGF-ß1/Smad2 signal path.

The nonpeptide AVE0991 attenuates myocardial hypertrophy as induced by angiotensin II through downregulation of transforming growth factor-beta1/Smad2 expression.

The nonpeptide AVE0991 is expected to be a putative new drug for cardiovascular diseases. However, the mechanisms for the cardioprotective actions of AVE0991 are still not fully understood. We planned to determine whether AVE0991 attenuates the angiotensin II (AngII)-induced myocardial hypertrophy and whether these AVE0991 effects involved transforming growth factor beta1 (TGF-beta1) and Smad2. A rat model of neonatal myocardial hypertrophy was induced by AngII. The AngII group significantly increased in protein content, surface area, and [(3)H]leucine incorporation efficiency by cardiomyocytes, compared to those of the control group (P < 0.01). The AngII group also had elevated TGF-beta1 and Smad2 expression (P < 0.01). These AngII-induced changes were significantly attenuated by AVE0991 in a dose-dependent manner. In our study, these actions of AngII (10(-6) mol/l) were significantly inhibited by both concentrations of AVE0991 (10(-5) mol/l and 10(-7) mol/l). Moreover, the high AVE0991 group had significantly better inhibition of myocardial hypertrophy than the low AVE0991 group. Meanwhile, the beneficial effects of AVE0991 were completely abolished when the cardiomyocytes were pretreated with Ang-(1-7) receptor antagonist A-779 (10(-6) mol/l). These results suggested that AVE0991 prevented AngII-inducing myocardial hypertrophy in a dose-dependent fashion, a process that may be associated with the inhibition of TGF-beta1/Smad2 signaling.

B-type natriuretic peptide attenuates cardiac hypertrophy via the transforming growth factor-ß1/smad7 pathway in vivo and in vitro.

1. Previously, we showed that long-term treatment of rats after myocardial infarction (MI) with B-type natriuretic peptide (BNP) prevented ventricular remodelling. However, it is unclear whether long-term BNP treatment affects cardiac hypertrophy and, if so, its mechanism of action. In the present study, we investigated the effects of long-term BNP treatment on cardiac hypertrophy and the molecular mechanisms involved. 2. Cardiac hypertrophy was established in rats by ligation of the left anterior descending coronary artery. After treatment with BNP (5 or 15 microg/kg per day) for 8 weeks, indices of cardiac hypertrophy were determined. In separate in vitro experiments, cardiomyocyte hypertrophy was induced by treatment of cardiomyocytes with 10(-6) mol/L angiotensin (Ang) II for 48 h and cell surface area and [(3)H] incorporation were measured. Transforming growth factor (TGF)-beta1 and smad7 mRNA and protein expression in vivo and in vitro were detected using reverse transcription-polymerase chain reaction and western blotting. 3. Long-term BNP treatment dose-dependently attenuated cardiac hypertrophy and improved cardiac function in rats after MI. Furthermore, BNP attenuated the upregulation of TGF-beta1 and downregulation of smad7 mRNA and protein expression. The in vitro experiments further proved that BNP inhibited cardiac hypertrophy and changes in the TGF-beta1/smad7 pathway, which were completely blocked by the cyclic GMP-dependent protein kinase (PKG) inhibitor, KT5823 (cells were treated with 10(-6) mol/L KT5823 for 48 h). 4. The results of the present study demonstrate that long-term treatment of rats with BNP dose-dependently attenuates cardiac hypertrophy and that this is associated with downregulation of TGF-beta1 and upregulation of smad7 via PKG signalling. Long-term BNP treatment may be a new therapeutic strategy to prevent cardiac hypertrophy and progression to heart failure.