Whitfieldmccormick7393

Benefit of high-dose cytarabine (HD-AraC) for acute myeloid leukemia (AML) prior to allogeneic hematopoietic stem cell transplantation (allo-HSCT) remains unknown. We retrospectively analyzed data from 79 non-core-binding-factor AML patients who underwent allo-HSCT in their first complete remission (CR1). In univariate analysis, HD-AraC (≥4 g/m2/day) before allo-HSCT improved disease-free survival (DFS) (p = .018), overall survival (OS) (p = .029), and cumulative incidence of relapse (CIR) (p = .033). Four-year DFS, OS, and CIR of patients receiving and not receiving HD-AraC were 79% vs. this website 49%, 82% vs. 56%, and 18% vs. 42%, respectively. In multivariate analysis, HD-AraC was a positive prognostic factor for DFS (hazard ratio (HR) = 0.36, 95% confidence interval (CI) 0.14-0.88), OS (HR  =  0.37, 95% CI 0.14-0.99), and CIR (HR  =  0.38, 95% CI; 0.14-1.0). Our study demonstrates that HD-AraC before allo-HSCT at a dose ≥4 g/m2/day is effective for treating AML patients in CR1.In the absence of a proven effective vaccine preventing infection by SARS-CoV-2, or a proven drug to treat COVID-19, the positive results of passive immune therapy using convalescent serum provide a strong lead. We have developed a new class of tetravalent, biparatopic therapy, 89C8-ACE2. It combines the specificity of a monoclonal antibody (89C8) that recognizes the relatively conserved N-terminal domain of the viral Spike (S) glycoprotein, and the ectodomain of ACE2, which binds to the receptor-binding domain of S. This molecule shows exceptional performance in vitro, inhibiting the interaction of recombinant S1 to ACE2 and transduction of ACE2-overexpressing cells by S-pseudotyped lentivirus with IC50s substantially below 100 pM, and with potency approximately 100-fold greater than ACE2-Fc itself. Moreover, 89C8-ACE2 was able to neutralize authentic viral infection in a standard 96-h co-incubation assay at low nanomolar concentrations, making this class of molecule a promising lead for therapeutic applications.The Triticum pathotype of Magnaporthe oryzae (MoT) that causes wheat blast has not yet been reported in the U.S., but the closely related M. oryzae Lolium pathotype (MoL), also capable of inciting blast, is found in several wheat growing regions. Since the epidemiology of MoL-incited wheat blast is unknown, it is difficult to project where and under what conditions this pathogen may be of importance. To quantify conditions favorable for MoL infection and temporal development of wheat blast, separate cohorts of wheat spikes were spray or point inoculated at anthesis and immediately subjected to different combinations of temperature (TEMP; 20, 25, and 30°C) and 100% relative humidity (RH) duration (0, 3, 6, 12, 24, and 48 h). Blast developed under all tested conditions, with both incidence (INC) and severity (SEV) increasing over time. The effects of TEMP on angular-transformed INC and SEV (arcINC and arcSEV) were significant (P less then 0.05) in most cases, with the magnitude of the TEMP effect influenced by RH duration when spikes were spray-inoculated. Between 12 and 21 days after inoculation (DAI), there were significant, positive linear relationships between hours of high RH and arcINC and arcSEV at 25 and 30°C, but not at 20°C. The estimated rates of increase in transformed INC or SEV per hour increase in high RH duration were significantly higher at 30°C than at 25°C at 12 to 14 DAI, but not at 19 to 21 DAI. The highest estimated temporal rates of increase in INC and SEV and the shortest estimated incubation periods (5 to 8 days) occurred at 25 and 30°C, with 24 and 48 h of high RH immediately after inoculation. These results will contribute to ongoing efforts to better understand the epidemiology of wheat blast incited by MoL as well as MoT.Ormosia pinnata (Lour.) Merr. is an important tree used for landscape and plant recovery of barren slopes in China. During an investigation of plant disease on landscape trees in 2018, a dieback was observed on O. pinnata trees in Guangzhou, Guangdong Province, China. Symptoms were characterized by initial dryness of the twigs and eventual death of the whole branch of the tree. Isolations from symptomatic branches yielded 13 isolates including two main morphotypes. Pathogenicity tests showed that isolate GDOP1 from Type I caused dieback of O. pinnata. Based on morphological characteristics and molecular analysis of the internal transcribed spacer rDNA (ITS1-5.8S-ITS2) and partial sequence of the translation elongation factor 1α (EF1-α), the fungus causing dieback on O. pinnata was identified as Lasiodiplodia pseudotheobromae. This is the first report of L. pseudotheobromae infecting O. pinnata in the world.Autophagy is critical for plant defense against necrotrophic pathogens, which causes serious yield loss on crops. However, the post-translational regulatory mechanisms of autophagy pathway in plant resistance against necrotrophs remain poorly understood. In this study, we report that phosphorylation modification on ATG18a, a key regulator of autophagosome formation in Arabidopsis thaliana, constitutes a post-translation regulation of autophagy, which attenuates plant resistance against necrotrophic pathogens. We found that phosphorylation of ATG18a suppresses autophagosome formation and its subsequent delivery into the vacuole, which results in reduced autophagy activity and compromised plant resistance against Botrytis cinerea. In contrast, overexpression of ATG18a dephosphorylation-mimic form increases the accumulation of autophagosomes and complements the plant resistance of atg18a mutant against B. cinerea. Moreover, BAK1, a key regulator in plant resistance, was identified to physically interact with and sequence; PAMP pathogen-associated molecular pattern; PCR polymerase chain reaction; PE phosphatidylethanolamine; PRR pattern recognition receptor; PtdIns(3,5)P2 phosphatidylinositol (3,5)-biphosphate; PtdIns3P phosphatidylinositol 3-biphosphate; PTI PAMP-triggered immunity; qRT-PCR quantitative reverse transcription PCR; SnRK2.6 SNF1-related protein kinase 2.6 in A. thaliana; TORC1 the rapamycin-sensitive Tor complex1; TRAF tumor necrosis factor receptor-associated factor; WT wild type plant; Yc C-terminal fragment of YFP; YFP yellow fluorescent protein; Yn N-terminal fragment of YFP.