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Background: Aspirin, with its pleiotropic effects such as anti-inflammatory and anti-platelet aggregation, has been widely used for anti-inflammatory, analgesic, and cardiovascular diseases. However, the association between the use of aspirin before the intensive care unit (ICU) and clinical outcomes in critically ill patients with acute kidney injury (AKI) is unknown. Methods: Patients with AKI in this retrospective observational study were selected from the Marketplace for Medical Information in Intensive Care IV (MIMIC-IV). The association between aspirin intervention and 30-day mortality was assessed using Cox proportional hazards model. Logistic regression models were used to assess the association of aspirin intervention with the risks of intracranial hemorrhage, gastrointestinal bleeding and blood transfusion. The propensity score matching (PSM) method was adopted to balance the baseline variables. Sensitivity analysis was performed to validate the results by multiple interpolations for the missing data. Results: The study included 4237 pre-ICU aspirin users and 9745 non-users. In multivariate models, we found a decreased risk of mortality in those who received aspirin before ICU compared to those who did not (30-day:hazard ratio [HR], 0.70; 95% CI, 0.62–0.79; p < 0.001; 90-day:HR, 0.70; 95% CI, 0.63–0.77, p < 0.001; 180-day:HR, 0.72; 95%CI,0.65–0.79, p < 0.001). This benefit was consistent in the post-PSM analyses, sensitivity analyses, and subgroup analyses. Moreover, aspirin intervention was associated with a reduced risk of intracranial hemorrhage and gastrointestinal bleeding (HR, 0.16; 95% CI, 0.10–0.25; p < 0.001; HR, 0.59; 95% CI, 0.38–0.88, p = 0.012) after being adjusted by relating covariates, whereas with a increased risk of blood transfusion (HR, 1.28; 95% CI, 1.16–1.46; p < 0.001). Conclusion: Patients with AKI treated with aspirin before ICU admission might have reduced 30-day, 90-day and 180-day mortality without increasing the risk of intracranial hemorrhage (ICH) or gastrointestinal bleeding, but may increase the risk of transfusion.

Sulforaphane is a common antioxidant selectively abundant in cruciferous plants, which exhibits effective anti-cancer actions in control of tumorigenesis or progression of various cancers. A recent study has shown that sulforaphane attenuates the EGFR signaling pathway in non-small cell lung cancer （NSCLC）, suggesting its potential anti-metastatic effects. In this study we assessed the involvement of sulforaphane and miR-616-5p in epithelial-mesenchymal transition （EMT） and NSCLC metastasis. Sulforaphane suppressed the cell proliferation in human NSCLC cell lines H1299, 95C and 95D with IC50 values of 9.52±1.23, 9.04±1.90 and 17.35±2.03 μmol/L, respectively. At low concentrations （1-5 μmol/L）, sulforaphane dose-dependently inhibited the migration and invasion of 95D and H1299 cells with relatively high metastatic potential. The anti-metastatic action of sulforaphane was confirmed in 95D and H1299 cell xenografts in vivo. In fresh NSCLC tissue samples from 179 patients, miR-616-5p levels were upregulated in late-stage NSCLCs, and strongly correlated with risk of NSCLC recurrence and metastasis. Consistent with the clinic observation, miR- 616-5p levels in the 3 NSCLC cell lines were correlated with their metastatic ability, and were decreased by sulforaphane treatment. Silencing miR-616-5p markedly suppressed the migration and invasion of 95D cells in vitro and NSCLC metastasis in vivo. Further studies revealed that miR-616-5p directly targeted GSK313 and decreased its expression, whereas sulforaphane decreased miR-616-5p levels by histone modification, and followed by inactivation of the GSK3β/β-catenin signaling pathway and inhibition of EMT, which was characterized by loss of epithelial markers and acquisition of a mesenchymal phenotype in NSCLC cells. Our findings suggest that sulforaphane is a potential adjuvant chemotherapeutic agent for the prevention of NSCLC recurrence and metastasis, and miR-616-5p can be clinically utilized as a biomarker or therapeutic target to inhibit metastasis.

Conventional organic solar cell’s (OSC) architectures, including rigid transparent substrate (Glass), conductive electrode (Indium tin oxide, ITO) and small working areas, are widely utilized in organic photovoltaic fields. However, such a structure as well as conventional spin-coating method obviously restrict their industrial application. In this article, we report the deposition of silver nanowires (AgNWs) on the flexible substrate by slot-die printing. The obtained AgNWs films exhibited a high transmittance and a low resistance, and were further used as the transparent conductive electrode of OSCs. A typical conjugated polymer, poly[(2,5-bis(2-hexyldecyloxy)phenylene)-alt-(5,6-difluoro-4,7-di(thiophen-2-yl)benzo[c] [1,2,5]thiadiazole)] (PPDT2FBT), was used as the active material to fabricate large-area (7 cm2 solar cells by a slot-die coating process. The power conversion efficiency (PCE) could reach 1.87% initially and further increased to 3.04% by thermal annealing. Compared to the performance of reference cell on ITO substrate, the result indicated that the AgNWs could be developed as an alternative substitute of conductive electrode to fabricate the large-area flexible OSCs by roll-to-roll printing.

Many stems are subject to shoot drying in the plantations of Calamus simplicifolius Wei at the Nanmeiling Base of the Forestry Bureau of Baisha County, Hainan Province. As a palm, stems of C simplicifolius stop growing and later die if the shoots are dry. Generally, shoot drying means reduced cane production and reduced profit for a rattan plantation. We aimed to quantify the incidence of shoot drying and determine its reason. We sampled eight 20 m × 20 m plots in the C simplicifolius plantations. In each plot, we counted stems and categorized them as drying shoot or normal shoot, and mother stem or sucker stem. We measured stem length and categorized them as drying shoot and normal shoot for mother stems. We cut open each shoot-drying stem to determine the cause of drying from drying part to fresh part. The frequency of mother stems （259 stem·ha^-1）, was significantly lower than sucker stems （588 stem·ha^-1）. The percentage of shoot drying was 33.8% for mother stems, not significantly higher than that for sucker stems （18,9%）. The mother shoot stems were significantly shorter if they were drying than if normal. 80% of stems with a drying shoot were hollow within the leaf sheath, whereas 10% hosted lively mature larvae （one larvae per shoot） and 10% hosted several lively young larvae. Mature larvae were identified as the Red Palm Weevil, Rhynchophorus ferrugineus Oliver. To confirm the present of the weevil, three pheromone traps for the weevil were set up in the plantations and adult weevils were trapped on the next day and identified as the Red Palm Weevil. We conclude that shoot drying of C. simplicifolius is probably caused by the Red Palm Weevil.

Human spermatozoa encounter an osmotic decrease from 330 to 290 mOsm I-z when passing through the female reproductive tract. We aimed to evaluate the role of chloride channels in volume regulation and sperm motility from patients with asthenozoospermia. Spermatozoa were purified using Percoll density gradients. Sperm volume was measured as the forward scatter signal using flow cytometry. Sperm motility was analyzed using computer-aided sperm analysis （CASA）. When transferred from an isotonic solution （330 mOsm I-z） to a hypotonic solution （290 mOsm I-Z）, cell volume was not changed in spermatozoa from normozoospermic men; but increased in those from asthenozoospermic samples. The addition of the chloride channel blockers, 4,4＇-diisothiocyanatostilbene-2,2＇- isulfonic acid （DIDS） or 5-nitro-2-（3-phenylpropylamino） benzoic acid （NPPB） to the hypotonic solution caused the normal spermatozoa to swell but did not increase the volume of those from the asthenozoospermic semen. DIDS and NPPB decreased sperm motility in both sets of semen samples. The inhibitory effect of NPPB on normal sperm motility was much stronger than on spermatozoa from the asthenozoospermic samples. Both sperm types expressed CIC-3 chloride channels, but the expression levels in the asthenozoospermic samples were much lower, especially in the neck and mid-piece areas. Spermatozoa from men with asthenozoospermia demonstrated lower volume regulating capacity, mobility, and CIC-3 expression levels （especially in the neck） than did normal spermatozoa. Thus, chloride channels play important roles in the regulation of sperm volume and motility and are downregulated in cases of asthenozoospermia.

The aim of this study was to determine whether the lower urinary tract storage symptoms of benign prostatic obstruction （BPO） could be completely resolved after plasmakinetic enucleation of the prostate （PKEP） and the possible predictors of persistent symptoms. Two hundred and sixty-seven cases of BPO performed PKEP from July 2008 to June 2009 were retrospectively analyzed. Five-year postoperative data were collected and compared with the preoperative data. According to the urodynamic results, the patients were divided into involuntary detrusor contraction （IDC） group （n = 95） and no IDC group （n = 172） preoperatively; the patients with IDC were divided into IDC-persistent group （n = 33） and IDC-resolved group （n = 62） after PKER The predictors of persistent IDC were analyzed. Compared with the preoperative data, the 5-year postoperative data showed that the IDC rate was lower （P --- 0.000）, Overactive Bladder Symptom Score （OABSS） was lower （P = 0.000）, maximum cystometric capacity （MCC） was larger （P= 0.000）, Prostate volume （PV） was smaller （P= 0.000）, and prostate-specific antigen （PSA） was lower （P= 0.000）. Compared with the no IDC group, the IDC group showed that the age was older （P = 0.016）, MCC was smaller （P = 0.004）, PSA was higher （P = 0.016）, and Chronic Inflammation rate was higher （P = 0.004）. Compared with IDC-resolved group after PKER IDC-persistent group showed that the age was older （P = 0.019）, MCC was smaller （P = 0.000）, PSA was higher （P = 0.013）, and Chronic Ihflammation rate was higher （P = 0.032）. The present study shows that the storage symptoms are still needed to be focused on after PKER The advanced patient age, MCC, PSA, and chronic inflammation may be the important clinical predictors of persistent IDC.

Ischemic stroke represents a significant danger to human beings, especially the elderly. Interventions are only available to remove the clot, and the mechanism of neuronal death during ischemic stroke is still in debate. Ferroptosis is increasingly appreciated as a mechanism of cell death after ischemia in various organs. Here we report that the serine protease, thrombin, instigates ferroptotic signaling by promoting arachidonic acid mobilization and subsequent esterification by the ferroptotic gene, acyl-CoA synthetase long-chain family member 4 (ACSL4). An unbiased multi-omics approach identified thrombin and ACSL4 genes/proteins, and their pro-ferroptotic phosphatidylethanolamine lipid products, as prominently altered upon the middle cerebral artery occlusion in rodents. Genetically or pharmacologically inhibiting multiple points in this pathway attenuated outcomes of models of ischemia in vitro and in vivo. Therefore, the thrombin-ACSL4 axis may be a key therapeutic target to ameliorate ferroptotic neuronal injury during ischemic stroke.

The regulation of adaptive responses to phosphorus (P) deficiency by the microRNA399 (miR399)/PHOSPHATE2 (PHO2) pathway has been well studied in Arabidopsis (Arabidopsis thaliana) but not in maize (Zea mays). Here, we show that miR399 transcripts are strongly induced in maize by phosphate (Pi) deficiency. Transgenic maize plants that overexpressed MIR399b accumulated excessive amounts of P in their shoots and displayed typical Pi-toxicity phenotypes. We reannotated ZmPHO2 with an additional 1,165 bp of the 5′ untranslated region. miR399-guided posttranscriptional repression of ZmPHO2 was mainly observed in the P-efficient lines. We identified Pi-deficiency-induced long-noncoding RNA1 (PILNCR1) from our strand-specific RNA libraries. Transient expression assays in Nicotiana benthamiana and maize leaf protoplasts demonstrated that PILNCR1 inhibits ZmmiR399-guided cleavage of ZmPHO2. The abundance of PILNCR1 was significantly higher in P-inefficient lines than in P-efficient lines, which is consistent with the abundance of ZmmiR399 transcripts. These results indicate that the interaction between PILNCR1 and miR399 is important for tolerance to low Pi in maize.

Congenital heart defects constitute the most common human birth defect, however understanding of how these disorders originate is limited by our ability to model the human heart accurately in vitro. Here we report a method to generate developmentally relevant human heart organoids by self-assembly using human pluripotent stem cells. Our procedure is fully defined, efficient, reproducible, and compatible with high-content approaches. Organoids are generated through a three-step Wnt signaling modulation strategy using chemical inhibitors and growth factors. Heart organoids are comparable to age-matched human fetal cardiac tissues at the transcriptomic, structural, and cellular level. They develop sophisticated internal chambers with well-organized multi-lineage cardiac cell types, recapitulate heart field formation and atrioventricular specification, develop a complex vasculature, and exhibit robust functional activity. We also show that our organoid platform can recreate complex metabolic disorders associated with congenital heart defects, as demonstrated by an in vitro model of pregestational diabetes-induced congenital heart defects. There is a pressing need to develop representative organ-like platforms recapitulating complex in vivo phenotypes to study human development and disease in vitro. Here the authors present a method to generate human heart organoids by self-assembly using pluripotent stem cells, compare these to age-matched fetal cardiac tissues and recreate a model of pregestational diabetes.

Let D be any division ring, and let T（mi,ni,k） be the set of k × k （k ≥ 2） rectangular block triangular matrices over D. For A, B ∈ T（mi,ni,k）, if rank（A - B） = 1, then A and B are said to be adjacent and denoted by A -B. A map T ： T（mi,ni,k） -〉 T（mi,ni,k） is said to be an adjacency preserving map in both directions if A - B if and only if φ（A） φ（B）. Let G be the transformation group of all adjacency preserving bijections in both directions on T（mi,ni,k）. When m1,nk ≥ 2, we characterize the algebraic structure of G, and obtain the fundamental theorem of rectangular block triangular matrices over D.