Background The outbreak of the coronavirus disease 2019 (Covid‐19) has shown a global spreading trend. Early and effective predictors of clinical outcomes are urgently needed to improve management of Covid‐19 patients. Objective The aim of the present study was to evaluate whether elevated D‐dimer levels could predict mortality in patients with Covid‐19. Methods Patients with laboratory confirmed Covid‐19 were retrospective enrolled in Wuhan Asia General Hospital from January 12, 2020, to March 15, 2020. D‐dimer levels on admission and death events were collected to calculate the optimum cutoff using receiver operating characteristic curves. According to the cutoff, the subjects were divided into two groups. Then the in‐hospital mortality between two groups were compared to assess the predictive value of D‐dimer level. Results A total of 343 eligible patients were enrolled in the study. The optimum cutoff value of D‐dimer to predict in‐hospital mortality was 2.0 µg/mL with a sensitivity of 92.3% and a specificity of 83.3%. There were 67 patients with D‐dimer ≥2.0 µg/mL, and 267 patients with D‐dimer <2.0 µg/mL on admission. 13 deaths occurred during hospitalization. Patients with D‐dimer levels ≥2.0 µg/mL had a higher incidence of mortality when comparing with those who with D‐dimer levels <2.0 µg/mL (12/67 vs 1/267, P < .001; hazard ratio, 51.5; 95% confidence interval, 12.9‐206.7). Conclusions D‐dimer on admission greater than 2.0 µg/mL (fourfold increase) could effectively predict in‐hospital mortality in patients with Covid‐19, which indicated D‐dimer could be an early and helpful marker to improve management of Covid‐19 patients. (Chinese Clinical Trial Registry: ChiCTR2000031428).
Changes of histone modification status at critical lineage-specifying gene loci in multipotent precursors can influence cell fate commitment. The contribution of these epigenetic mechanisms to natural killer (NK) cell lineage determination from common lymphoid precursors is not understood. Here we investigate the impact of histone methylation repressive marks (H3 Lys27 trimethylation; H3K27 me3 ) on early NK cell differentiation. We demonstrate that selective loss of the histone-lysine N-methyltransferase Ezh2 (enhancer of zeste homolog 2) or inhibition of its enzymatic activity with small molecules unexpectedly increased generation of the IL-15 receptor (IL-15R) CD122 + NK precursors and mature NK progeny from both mouse and human hematopoietic stem and progenitor cells. Mechanistic studies revealed that enhanced NK cell expansion and cytotoxicity against tumor cells were associated with up-regulation of CD122 and the C-type lectin receptor NKG2D. Moreover, NKG2D deficiency diminished the positive effects of Ezh2 inhibitors on NK cell commitment. Identification of the contribution of Ezh2 to NK lineage specification and function reveals an epigenetic-based mechanism that regulates NK cell development and provides insight into the clinical application of Ezh2 inhibitors in NK-based cancer immunotherapies.epigenetic regulation | NKG2D | hematopoietic stem and progenitor cells | histone modification | innate immunity
The self-assembly and electrochemical properties of a series of thiol-functionalized anthraquinone derivatives were studied on gold by cyclic voltammetry. The compounds were l,8-bis(l,7-dithia-4-oxaheptyl)anthracene-9,10-dione (1), l,8-bis(4,7-dioxa-l,10-dithiadecyl)anthracene-9,10-dione (2), and l-(4,7-dioxal,10-dithiadecyl)anthracene-9,10-dione (3). Compounds 1-3 formed self-assembled monolayers on gold with surface coverages of 2.7 X Kb10, 2.5 X 10~10, and 2.9 x 10"10 mol/cm1 2, respectively. All monolayers showed voltammetric responses in 0.1 KOH that corresponded to the two-electron reduction of the anthraquinone subunit. However, the voltammetric response was not reversible, exhibiting large peakto-peak potential splittings (60-80 mV at a scan rate of 0.1 V/s) and other distortions. The voltammetric reversibility increased substantially in mixed monolayers prepared by the competitive self-assembly of one of the anthraquinone derivatives and a 1-alkanethiol (Ci0 to C18). Interestingly, the anthraquinone derivatives competed quite effectively with alkanethiols for adsorption sites on the gold surface. Compound 2 was found to be optimum in this regard because it has two thiol-terminated chains that may serve as anchoring points to the gold surface.
The purpose of this study was to explore how the mitochondrial AOX (alternative oxidase) pathway alleviates photoinhibition in Rumex K-1 leaves. Inhibition of the AOX pathway decreased the initial activity of NADP-malate dehydrogenase (EC 1.1.1.82, NADP-MDH) and the pool size of photosynthetic end electron acceptors, resulting in an over-reduction of the photosystem I (PSI) acceptor side. The over-reduction of the PSI acceptor side further inhibited electron transport from the photosystem II (PSII) reaction centers to the PSII acceptor side as indicated by an increase in V(J) (the relative variable fluorescence at J-step), causing an imbalance between photosynthetic light absorption and energy utilization per active reaction center (RC) under high light, which led to the over-excitation of the PSII reaction centers. The over-reduction of the PSI acceptor side and the over-excitation of the PSII reaction centers enhanced the accumulation of reactive oxygen species (ROS), which inhibited the repair of the photodamaged PSII. However, the inhibition of the AOX pathway did not change the level of photoinhibition under high light in the presence of the chloroplast D1 protein synthesis inhibitor chloramphenicol, indicating that the inhibition of the AOX pathway did not accelerate the photodamage to PSII directly. All these results suggest that the AOX pathway plays an important role in the protection of plants against photoinhibition by minimizing the inhibition of the repair of the photodamaged PSII through preventing the over-production of ROS.
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