Carbon sequestration potential and its main drivers in soils under alfalfa (Medicago sativa L.).

As a perennial forage crop, alfalfa (Medicago sativa L.) has been extensively utilized for the vegetation restoration of degraded soil and provides feedstock for forage. Its high usage can be attributed to its high yield potential and the increasing soil organic carbon (SOC) sequestration of alfalfa cultivation. However, the impact of land conversion to alfalfa on SOC content and its underlying drivers remain unclear. We performed a meta-analysis at the global scale to explore the quantified effects of alfalfa cultivation on SOC content and identify its controlling factors. We employed 1699 pairwise data points from 90 publications based on cropland/abandoned land conversion to alfalfa. Globally, cropland (cropland-alfalfa) and abandoned land (abandoned land-alfalfa) conversion to alfalfa enhanced SOC content by 12.1 % and 13.7 %, respectively. Alfalfa exhibited greater SOC content benefits in the surface soils (0-20 cm) with a lower level of initial SOC (<16 g kg-1), regardless of the land conversion type. Cropland-alfalfa was observed to increase SOC content with fertilization, irrigation, and conventional tillage in the long term (>5 years). Furthermore, abandoned land-alfalfa enhanced SOC content in the absence of alfalfa biomass removal and for longer cultivation durations (>5 years). Boosted regression tree analyses indicated variations in soil properties (75 % for cropland-alfalfa and 65 % for abandoned land-alfalfa) as the primary factors driving changes in SOC content. The dominant drivers were determined as the soil layer (51.6 %), cultivation duration (13.1 %), and initial SOC (12.9 %) for cropland-alfalfa, and initial SOC (43.7 %), soil layer (24.6 %) and cultivation duration (17.1 %) for abandoned land-alfalfa. Land conversion to alfalfa has great potential for SOC sequestration, particularly in low-fertility soils. Therefore, alfalfa cultivation is highly recommended for degraded lands due to its SOC sequestration benefits in vegetation restoration.

Application of an autotransfusion pressure control system in blood salvage.

OBJECTIVE: This study was performed to evaluate the effect of a homemade autotransfusion pressure-control system on the regulation of negative pressure and to clarify the influence of different negative pressures on the recovered erythrocytes. METHODS: Fifty patients were randomly divided into five groups, and five different suction-generated negative pressures were applied. Before suction, 6 mL of blood was collected from the surgical field; after suction, 6 mL of blood was collected from the blood storage tank. The hemoglobin, hematocrit, mean corpuscular volume, newly generated standardized plasma free hemoglobin, and change in the hemolysis rate of erythrocytes before and after suction were compared. Additionally, the erythrocyte morphology was observed. RESULTS: The hemoglobin and hematocrit were significantly different before and after suction in all five groups. As the suction pressure increased, gradual increases were noted in the number of abnormal erythrocytes in the field of view, the newly generated standardized plasma free hemoglobin, and the change in the hemolysis rate. CONCLUSIONS: The destruction rate of erythrocytes increased as the suction-generated negative pressure increased. When using a pressure-control system, a negative pressure of <200 mmHg should be applied to reduce the damage to the autotransfused blood.

Efficacy and Safety of Ciprofol for Sedation/Anesthesia in Patients Undergoing Hysteroscopy: A Randomized, Parallel-Group, Controlled Trial.

Objective: To compare the efficacy and safety of ciprofol and propofol for sedation during hysteroscopy. Methods: A total of 149 patients undergoing hysteroscopy were randomly assigned to a ciprofol (Group C) or propofol group (Group P). All cases received intravenous sufentanil 0.1 µg/kg for analgesic preconditioning. Group C received an induction dose of ciprofol 0.4 mg/kg and a maintenance dosage of 0.6-1.2 mg/kg/h to maintain BIS value between 40-60. In Group P, propofol was started at 2.0 mg/kg and then maintained at 3.0-6.0 mg/kg/h. The primary outcome was the successful rate of hysteroscopy. Secondary outcomes included the change of hemodynamic, respiratory adverse events, injection pain, body movement, recovery time, anesthetist's satisfaction, time of disappearance of the eyelash reflex and the incidence of nausea and vomiting. Results: The success rate of hysteroscopy in each group was 100%. After drug administration, the incidence of hypotension in Group C was much lower than that in Group P (P< 0.05). The incidence of respiratory adverse events in Group C (4.0%) was much lower than that in Group P (31.1%) (P< 0.05). The incidence of injection pain and body movement in Group C was significantly lower than that in Group P (P< 0.05). The mean eyelash reflex disappearance time was less than 3 minutes in both groups. There was no statistically significant difference between the two groups in awakening times, anesthetist's satisfaction and the incidence of nausea and vomiting. No serious adverse events occurred in any patients. Conclusion: Ciprofol proved to be a safer alternative to propofol for anesthesia during hysteroscopy. In comparison to propofol, ciprofol does not cause injection pain, exerts less impact on hemodynamics, and results in less respiratory depression.

Clinical effect of different doses of ciprofol for induction of general anesthesia in elderly patients: A randomized, controlled trial.

Ciprofol is a newly developed intravenous anesthetic agent with improved pharmacokinetic properties. Compared to propofol, ciprofol exhibits stronger binding to the GABAA receptor and elicits a greater enhancement of GABAA receptor-mediated neuronal currents in vitro. The aims of the present clinical trials were to examine the safety and efficacy of different doses of ciprofol for induction of general anesthesia in elderly patients. A total of 105 elderly patients undergoing elective surgery were randomized, in a 1:1:1 ratio, to receive one of three sedation regimens: (1) the C1 group (0.2 mg/kg ciprofol), (2) the C2 group (0.3 mg/kg ciprofol), (3) the C3 group (0.4 mg/kg ciprofol). The primary outcome was the incidence of various adverse events, including hypotension, hypertension, bradycardia, tachycardia, hypoxemia, and injection pain. The secondary outcomes of efficacy were the success rate of general anesthesia induction, the time to anesthesia induction, and the frequency of remedial sedation was recorded in each group. Adverse events occurred in 13 patients (37%) in group C1, 8 patients (22%) in group C2, and 24 patients (68%) in group C3. Compared with group C2, the total incidence of adverse events was significantly higher in group C1 and group C3 (p < .001).The success rate of general anesthesia induction in the three groups was 100%. Compared with group C1, the frequency of remedial sedation was significantly lower in group C2 and group C3. The outcomes demonstrated that ciprofol at a dose of 0.3 mg/kg has good safety and efficacy in the induction of general anesthesia in elderly patients. Overall, ciprofol is a new and viable option for the induction of general anesthesia in elderly patients undergoing elective surgery.

Dexmedetomidine reduces dextran sulfate sodium (DSS)-induced NCM460 cell inflammation and barrier damage by inhibiting RhoA/ROCK signaling pathway.

OBJECTIVE: This study investigated the role of dexmedetomidine (DEX) in dextran sulfate sodium (DSS)-induced NCM460 cells. MATERIAL AND METHODS: The viability and apoptosis of NCM460 cells treated with DEX with or without DSS were detected by CCK-8 and terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) assay. The level of inflammatory factors and expression of inflammation-related proteins, tight junction proteins and Ras homolog gene family, member A/Rho-associated coiled-coil containing protein kinase (RhoA/ROCK) signaling-related proteins in NCM460 cells treated with DEX and/or U46619 (RhoA/ROCK agonist) and/or DSS were detected by the respective enzyme-linked immunosorbent assay (ELISA) kits and Western blot analysis. The permeability of NCM460 monolayers was examined with transepithelial electrical resistance (TEER) assay. RESULTS: DEX had no effect on NCM460 cell viability. However, DEX improved the viability and barrier damage and suppressed the apoptosis and inflammation of DSS-induced NCM460 cells. Correspondingly, the expression of inflammation-related proteins was reduced and the expression of tight junction proteins was increased in DSS-induced NCM460 cells after treatment with DEX. In addition, RhoA/ROCK signaling was activated in NCM460 cells induced by DSS, which was suppressed by DEX. The protective effects of DEX on DSS-indued NCM460 cells were reversed by U46619. CONCLUSION: DEX improved viability and barrier damage while suppressed apoptosis and inflammation in DSS-indued NCM460 cells by inhibiting RhoA/ROCK signaling pathway.

The mechanism of sevoflurane post-treatment alleviating hypoxic-ischemic encephalopathy by affecting histone methyltransferase G9a in rats.

Hypoxic-ischemic encephalopathy (HIE) is recognized as the main cause of neonatal death, and efficient treatment strategies remain limited. This study aims to investigate the mechanism of sevoflurane (SF) post-treatment in alleviating HIE in rats. The HIE rat model and oxygen-glucose deprivation (OGD) cell model were established, and adeno-associated virus (AAV)-histone-lysine N-methyltransferase EHMT2 (G9a) was transfected after SF treatment. The learning and memory ability and the levels of nerve growth factor (NGF)/brain-derived neurotrophic factor (BDNF) were evaluated and determined. The levels of G9a/histone H3 lysine 9 dimethylation (H3K9me2) and the enrichment level of H3K9me2 in the promoter region of BDNF gene were analyzed. After SF post-treatment, the neurons in cerebral cortex, the learning and memory skills and the contents of NGF/BDNF were increased, while the apoptosis and G9a/H3K9me2 levels were reduced. After overexpression of G9a in vitro/vivo, the enrichment levels of H3K9me2 in the promoter region of BDNF were increased, the levels of BDNF were decreased, the neurons were damaged and the learning and memory abilities of HIE rats were impaired. The conclusion is that SF post-treatment can promote the expression of BDNF by inhibiting H3K9me2 on the BDNF gene promoter and inhibiting G9a, thus alleviating HIE in rats.

Trends in Disease Burden Attributable to Tobacco in China, 1990-2017: Findings From the Global Burden of Disease Study 2017.

In 2018, there were more than 371 million cigarette smokers and 12. 6 million electronic cigarette users, with 340.2 million non-smokers exposed to secondhand smoke (SHS) in China, which resulted in heavy tobacco-attributable disease burden. According to the definition by the Global Burden of Disease Study 2017 (GBD 2017), tobacco is a level 2 risk factor that consists of three sublevel risk factors, namely, smoking, SHS, and chewing tobacco. In this study, we aimed to evaluate the trends in deaths and disability-adjusted life years (DALYs) attributable to tobacco, smoking, SHS, and chewing tobacco by sex in China from 1990 to 2017 and to explore the leading causes of tobacco-attributable deaths and DALYs using data from the GBD 2017. From 1990 to 2017, the tobacco-attributable death rates per 100,000 people decreased from 75.65 [95% uncertainty interval (95% UI) = 56.23-97.74] to 70.90 (95% UI = 59.67-83.72) in females and increased from 198.83 (95% UI = 181.39-217.47) to 292.39 (95% UI = 271.28-313.76) in males. From 1990 to 2017, the tobacco-attributable DALY rates decreased from 2209.11 (95% UI = 1678.63-2791.91) to 1489.05 (95% UI = 1237.65-1752.57) in females and increased from 5650.42 (95% UI = 5070.06-6264.39) to 6994.02 (95% UI = 6489.84-7558.41) in males. In 2017, the tobacco-attributable deaths in China were concentrated on chronic obstructive pulmonary disease, ischemic heart disease, lung cancer, and stroke. The focus of tobacco control for females was SHS in 1990, whereas smoking and SHS were equally important for tobacco control in females in 2017. Increasing tobacco taxes and prices may be the most effective and feasible measure to reduce tobacco-attributable disease burdens.

A portable internal contamination monitor with dual detectors for screening in a large-scale radiological incident.

In the case of a radiological incident, large numbers of affected people should get rapid internal contamination screening, so a portable internal contamination monitor for large-scale application has been developed. It comprises dual detectors, a digital gamma spectrometer, and analysis software. Experiments carried out with a Chinese adult man model. Because of the inadequate shielding and poor detector resolution, the monitor is not sensitive to the lower energy emitters. However, it shows the excellent performance for the emitters above 661 keV. MDA for Cs-137, Y-88, and Co-60 reached 320Bq, 300Bq, and 530Bq in 5-min measurement. Due to the strong mobility, considerable detection limit, and low cost, the monitor can be applied to the rapid internal contamination screening in a radiological incident.

Sevoflurane inhibits the migration and invasion of colorectal cancer cells through regulating ERK/MMP-9 pathway by up-regulating miR-203.

Surgery resection is the primary treatment for colorectal cancer (CRC) patients with the risk of cancer dissemination and metastasis. Sevoflurane is one inhalational anesthesia which regulates migration and invasion in varying cancers. However, the effect of sevoflurane on CRC cells and its mechanism remain poorly understood. In this study, SW620 and HCT116 cells were treated with different concentrations of sevoflurane for 6 h in vitro. We measured the effect of sevoflurane on cell survival, migration and invasion by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide or trans-well assays. Moreover, we explored the interaction between sevoflurane and miR-203 and Roundabout1 (Robo1) as well as the extracellular signal-regulated kinase (ERK) and matrix metalloproteinase-9 (MMP-9) pathway. Results showed that sevoflurane inhibited cell migration and invasion in SW620 and HCT116 cells in a concentration dependent manner. Moreover, different concentrations of sevoflurane suppressed the phosphorylation of ERK. miR-203 expression was impaired while sevoflurane reversed the expression of miR-203 in CRC cells. In addition, inhibition of miR-203 attenuated the inhibitory effect of sevoflurane on cell migration, invasion and phosphorylated ERK level. Notably, MMP-9, as a downstream of ERK, was involved in sevoflurane-mediated processes in CRC cells. Besides, Robo1 was indicated as a target of miR-203 and inhibited by sevoflurane treatment. These results indicated that sevoflurane suppressed cell migration and invasion through regulating ERK/MMP-9 pathway via miR-203/Robo1 in CRC cells, indicating important clinical implications for anesthetic agents to prevent metastasis in CRC.

Sevoflurane Ameliorates Myocardial Cell Injury by Inducing Autophagy via the Deacetylation of LC3 by SIRT1.

Misfolded and aberrant proteins have been found to be associated with myocardial cell injury. Thus, increased clearance of misfolded or aggregated proteins via autophagy might be a potential option in preventing myocardial cell injury. Sevoflurane may ameliorate myocardial cell injury by affecting sirtuin 1- (SIRT1-) mediated autophagy. Rat models with myocardial cell injury were induced by limb ischemia reperfusion. The model rats received different treatments: sevoflurane, nicotinamide, and autophagy inhibitor 3-methyladenine (3-MA). Autophagy was observed by SEM. The levels of SIRT1 and microtubule-associated protein 1A/1B-light chain 3 (LC3) were measured. Present findings demonstrated that limb ischemia reperfusion induced autophagy. Sevoflurane increased the level of SIRT1, which deacetylated LC3 and further increased autophagic rates. On the other hand, the autophagy was inhibited by sevoflurane and or the inhibitors of SIRT1 and LC3. Present results demonstrated a novel molecular mechanism by which sevoflurane induced autophagy by increasing the level of SIRT1 and reducing the acetylation of LC3.

Sevoflurane ameliorates doxorubicin-induced myocardial injury by affecting the phosphorylation states of proteins in PI3K/Akt/mTOR signaling pathway.

BACKGROUND: The effect of sevoflurane on the doxorubicin-induced myocardial injury was explored by investigating the phosphorylation states of proteins in phosphatidylinositol 3-kinase (PI3K)/Akt/mam-malian target of rapamycin (mTOR) signaling pathway. METHODS: Myocardial injury rat models were induced by doxorubicin and evenly assigned into five groups according to different treatment: Doxorubicin group (DG, 200-µL saline solution), sevoflurane group (SevG, inhaled with 2.4% sevoflurane for 2 h), LY294002 group (LYG, Akt inhibitor, 0.3 mg/kg in 200-µL Dimethyl Sulfoxide [DMSO]), solvent DMSO control group (SG) and autophagy inhibitor 3-methyladenine (3-MA) group (MG, 30 mg/kg in 200-µL DMSO). The healthy rats were assigned to a contro1 group (CG, 200-µL saline solution). Myocardial apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The concentration of cardiac troponin I (cTnI) was detected by ELISA. The levels of total Akt (t-Akt), phosphorylated Akt (p-Akt), mammalian target of rapamycin (mTOR), phosphorylated-mTOR (p-mTOR) and autophagy marker LC3-II was detected by Western Blot. The experiments were also repeated at the cell level. RESULTS: Terminal deoxynucleotidyl transferase dUTP nick end labeling analysis showed that the ap-optosis rates were high in DG and SG, reached the highest level in LYG, reduced in SevG and MG, and reached the lowest level in CG. The levels of p-Akt p-mTOR were low in groups DG and SG, reached the lowest level in LYG, increased in SevG and MG, and reached the highest level in CG. In contrast, LC3-II expression, apoptosis index and serum cTnI concentration were high in DG and SG, reached the highest level in LYG, reduced in SevG and MG, and reached the lowest level in CG (p < 0.05). Cell experiment showed similar results as with animal experiments. CONCLUSIONS: Sevoflurane ameliorates myocardial injury by affecting the phosphorylation states of the proteins in PI3K/Akt/mTOR signaling pathway and reducing the injury biomarker. (Cardiol J 2017; 24, 4: 409-418).