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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.

In order to realize precise fertilization and high yield management of为实现马尾松无性系种子园精准施肥和丰产经营,用不同结实能力无性系作为材料,设置每株0、400、800和1600 g 4个磷肥水平(分别记为P

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 2/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.

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.

The central venous-to-arterial carbon dioxide difference (Pcv-aCOPatients with BSI admitted to the intensive care unit at Guangdong Provincial People's Hospital between August 2014 and August 2017 were enrolled. Pcv-aCOA total of 132 patients with BSI were enrolled. The Pcv-aCOPcv-aCO

Background: Around the globe, moderate cases account for the largest proportion of all COVID-19 patients, and deteriorated moderate patients contribute the most in mortality. However, published articles failed to address the deterioration details of moderate case, especially on when and how they deteriorated. Methods: All moderate COVID-19 patients hospitalized in Guangdong Province from Jan 14th to Mar 16th, 2020 were included in this multi-centre, retrospective, cohort study, and were divided into deteriorated and non-deteriorated groups according to clinical status. Demography, symptoms, therapy and laboratory characteristics were collected to explore the features of disease deterioration. Findings: Of 1168 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 (IQR 9-14). 12.2% severe cases could further develop to critical status after 3 days (IQR 2-6.5) of 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 showed (80.4%) SaO2 2.0mmol/L. In view of multiple organs 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 were occurred in deteriorated patients; while the organs injuries occurred in following sequence: ARDS, AKI, AHF, Coagulopathy, AHI and Shock. Interpretation: The deteriorated pattern of moderate COVID-19 patients is characterized as the 11th day from onset (IQR 9-14) being an important time point of disease deterioration with further exacerbate to critical condition in 3 days (IQR 2-6.5); and ARDS followed by AKI being the typical mode of sequential organs damage. Funding Statement: This study is supported by Special Project on Emergency Response to Control of Novel Coronavirus Infection of Guangdong Province (NO. 2020B1111330003) and National Natural Science Foundation of China (NO. 81701875). Declaration of Interests: All authors declare no competing interests. Ethics Approval Statement: The study was approved by the Institutional Review Board of Guangdong Health Commission and Guangdong Provincial People’s Hospital (No. GDREC2020028H). Written informed consent was waived in light of the urgent need to collect data.

Background: COVID-19 has already become a global pandemic There are few detailed descriptions of moderate cases and their clinical progression Our aim was to

Background: Recurrence of positive SARS-CoV-2 RNA in discharged COVID-19 patients attracts the public’s concern. It remained unknown whether this phenomenon means relapse of disease or transmissible, which is essential to the management of discharged COVID-19 patients. Methods: A multi-center, retrospective, observational study was conducted on 32 designated hospitals for COVID-19 in Guangdong Province. All COVID-19 discharged patients from January 14 th to March 10 th , 2020 were enrolled in this study, and were followed up for 14 days with testing of SARS-CoV-2 nucleic RNA, observation of clinical symptoms, chest CT scan and laboratory tests. Clinical symptoms and RNA test also were carried out in their close contacts. Findings: Of 1,282 discharged patients enrolled in this study, 155(12.1%)were tested positive of SARS-CoV-2 RNA during 14 days’ follow-up. The median time of recurrence of SARS-CoV-2 RNA was 7 days (IQR4-9). Compared to negative group, the patients from re-positive group were a younger (35yr vs 45yr mean,p

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)-1β. 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-1β 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-1β.

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 NTRTCT. 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.

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.

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.

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.

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.

The combination of isotope trace technique and SOC fractionation allows a better understanding of SOC dynamics. A five-year tillage experiment consisting of no-tillage (NT) and mouldboard plough (MP) was used to study the changes in particle-size SOC fractions and correspondingδ13C natural abundance to assess SOC turnover in the 0–20 cm layer of black soils under tillage practices. Compared to the initial level, total SOC tended to be stratified but showed a slight increase in the entire plough layer under short-term NT. MP had no significant impacts on SOC at any depth. Because of significant increases in coarse particulate organic carbon (POC) and decreases in fine POC, total POC did not remarkably decrease under NT and MP. A distinct increase in silt plus clay OC occurred in NT plots, but not in MP plots. However, theδ13C abundances of both coarse and fine POC increased, while those of silt plus clay OC remained almost the same under NT. The C derived from C3plants was mainly associated with fine particles and much less with coarse particles. These results suggested that short-term NT and MP preferentially enhanced the turnover of POC, which was considerably faster than that of silt plus clay OC.

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-β1 (TGF-β1)/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-β1/Smad2 signal path.

Summary 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 μg/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 [3H] incorporation were measured. Transforming growth factor (TGF)-β1 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-β1 and downregulation of smad7 mRNA and protein expression. The in vitro experiments further proved that BNP inhibited cardiac hypertrophy and changes in the TGF-β1/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-β1 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.

Although short-term B-type natriuretic peptide (BNP) treatment has been shown to be effective for decompensated congestive heart failure, little is known about the effects of long-term BNP treatment in ventricular remodeling and heart failure in response to myocardial infarction. The aim of the present study was to investigate the effects of long-term BNP treament on ventricular remodeling and heart failure after myocardial infarction in rats. Myocardial infarction was induced by ligating the left anterior descending coronary artery. The surviving rats were randomly divided into four groups: 1) vehicle-treated myocardial infarction group (‘vehicle-treated group’), 2) rats treated with low-dose BNP (‘low BNP group’), 3) rats treated with high-dose BNP (‘high BNP group’), 4) sham-operated group. Eight weeks after the operation, rats were sacrificed. Compared with the sham-operated group, the vehicle-treated group had significantly higher collagen deposition and angiotensin II levels (P < 0.01) and a significantly lower cardiac function (P < 0.05). Both BNP-treated groups had significant improvement of these indexes compared with the vehicle-treated group (P < 0.01). The high BNP group had significantly less collagen deposition and better cardiac function than the untreated and low BNP groups. Moreover, the mRNA and protein expression of TGFβ1 and Smad2 in the vehicle-treated group was significantly higher than in the sham-operated group (P < 0.01). Both BNP-treated groups had a suppression of TGFβ1 and Smad2 expression (P < 0.01). In conclusion, long-term treatment with BNP prevents ventricular remodeling and deterioration of cardiac function in a dose-dependent fashion, a process that may be associated with the inhibition of TGFβ1/ Smad2 signaling.