On Dissipative Radiative MHD Boundary Layer Flow in a Porous Medium Over a Non Isothermal Stretching Sheet

The paper aims at investigating the effects of Ohmic and viscous dissipations on the steady two-dimensional radiative boundary-layer flow of an incompressible, viscous, electrically conducting fluid caused by a linearly stretching sheet placed at the bottom of fluid saturated porous medium in the presence of uniform transverse magnetic field. The radiative heat flux is assumed to follow Rosseland approximation. The governing system of partial differential equations are converted to ordinary differential equations by using the similarity transformations, which are then solved numerically using shooting method with fourth order Runge-Kutta scheme. The dimensionless temperature distribution is computed for different thermo-physical parameters and presented graphically. The temperature gradient at the sheet and skin friction coefficient are derived numerically and presented through graph

Sufficiency criteria for a class of p-valent analytic functions of complex order

In this paper we obtain extensions of sufficient conditions for analytic functions f(z) in the open unit disk \mathcal{U} to be starlike and convex of complex order. Our results unify and extend some starlikeness and convexity conditions for analytic functions discussed by Mocanu [1988], Uyanik et al. [2011], Goyal et al. [2012] and others

A protocol for simultaneous high-sensitivity genotyping and chromatin accessibility profiling in single cells.

Single-cell assay for transposase-accessible chromatin with sequencing (scATAC-seq) resolves the heterogeneity of epigenetic states across cells but does not typically capture exonic mutations, which limits our knowledge of how somatic mutations alter chromatin landscapes. Here, we present a plate-based approach coupling high-sensitivity genotyping of genomic loci with high-content scATAC-seq libraries from the same single cells. We first describe steps for optimization of genotyping primers, followed by detailed guidance on the preparation of both scATAC-seq and single-cell genotyping libraries, fully automated on high-throughput liquid handling platforms. For complete details on the use and execution of this protocol, please refer to Turkalj, Jakobsen et al.

South-South Collaboration in CCAFS for developing capacity on weather index insurance

Climate risk management has become a key area for research and policy dialogue due to increasing threats of disasters and climate extremes, which are likely to increase due to climate change. Global south (including Latin America, Africa, South and South-east Asia) is a major hotspot for climatic risk challenges due to high exposure to climate extremes when compared to temperate regions, high incidences of poverty, poor enabling environments and low regulatory support. With this backdrop, the CGIAR Research Program Climate Change, Agriculture and Food Security (CCAFS) has been working in Africa, Latin America and Asia together with its partners on accelerating climatic risk management through a dedicated research flagship to Climate services and safety nets. A workshop was thus organized by CCAFS to mobilize stakeholders in different regions to facilitate the diffusion of learnings and advances in climate risk management from one region to another. This workshop was planned after feedback and follow-up from South: South collaboration on climatic risk management workshop in New York, concurrent with the needs and demands of the stakeholders

Enasidenib vs conventional care in older patients with late-stage mutant-IDH2 relapsed/refractory AML: a randomized phase 3 trial

Enasidenib; Conventional careEnasidenib; Atenció convencionalEnasidenib; Atención convencionalThis open-label, randomized, phase 3 trial (NCT02577406) compared enasidenib, an oral IDH2 (isocitrate dehydrogenase 2) inhibitor, with conventional care regimens (CCRs) in patients aged ≥60 years with late-stage, mutant-IDH2 acute myeloid leukemia (AML) relapsed/refractory (R/R) to 2 or 3 prior AML-directed therapies. Patients were first preselected to a CCR (azacitidine, intermediate-dose cytarabine, low-dose cytarabine, or supportive care) and then randomized (1:1) to enasidenib 100 mg per day or CCR. The primary endpoint was overall survival (OS). Secondary endpoints included event-free survival (EFS), time to treatment failure (TTF), overall response rate (ORR), hematologic improvement (HI), and transfusion independence (TI). Overall, 319 patients were randomized to enasidenib (n = 158) or CCR (n = 161). The median age was 71 years, median (range) enasidenib exposure was 142 days (3 to 1270), and CCR was 36 days (1 to 1166). One enasidenib (0.6%) and 20 CCR (12%) patients received no randomized treatment, and 30% and 43%, respectively, received subsequent AML-directed therapies during follow-up. The median OS with enasidenib vs CCR was 6.5 vs 6.2 months (HR [hazard ratio], 0.86; P = .23); 1-year survival was 37.5% vs 26.1%. Enasidenib meaningfully improved EFS (median, 4.9 vs 2.6 months with CCR; HR, 0.68; P = .008), TTF (median, 4.9 vs 1.9 months; HR, 0.53; P < .001), ORR (40.5% vs 9.9%; P <.001), HI (42.4% vs 11.2%), and red blood cell (RBC)-TI (31.7% vs 9.3%). Enasidenib safety was consistent with prior reports. The primary study endpoint was not met, but OS was confounded by early dropout and subsequent AML-directed therapies. Enasidenib provided meaningful benefits in EFS, TTF, ORR, HI, and RBC-TI in this heavily pretreated older mutant-IDH2 R/R AML population.This work was supported by Celgene, a Bristol-Myers Squibb Company

METHOD AND SYSTEM FOR MIGRATING A CODE FROM A FIRST FORMAT TO A SECOND FORMAT

The present disclosure relates to a migration tool to convert a code in a first format to a code in a second format. The source code received can be from a user (108) or from a database (106). The input code is said to be in the first format. An Abstract Syntax tree (AST) of the code in the first format is generated by a system (104) by parsing the code. A modified AST is generated based on the AST of the code in the first format. A code in the second format is generated from the modified AST

Heterogeneous leukemia stem cells in myeloid blast phase chronic myeloid leukemia

Chronic myeloid leukemia (CML) is an excellent model of the multistep processes in cancer. Initiating BCR-ABL mutations are required for the initial phase of the disease (chronic phase, CP-CML). Some CP-CML patients acquire additional mutation(s) that transforms CP-CML to poor prognosis, hard to treat, acute myeloid or lymphoid leukemia or blast phase CML (BP-CML). It is unclear where in the hemopoietic hierarchy additional mutations are acquired in BP-CML, how the hemopoietic hierarchy is altered as a consequence, and the cellular identity of the resulting leukemia-propagating stem cell (LSC) populations. Here, we show that myeloid BP-CML is associated with expanded populations that have the immunophenotype of normal progenitor populations that vary between patients. Serial transplantation in immunodeficient mice demonstrated functional LSCs reside in multiple populations with the immunophenotype of normal progenitor as well as stem cells. Multicolor fluorescence in situ hybridization detected serial acquisition of cytogenetic abnormalities of chromosome 17, associated with transformation to BP-CML, that is detected with equal frequency in all functional LSC compartments. New effective myeloid BP-CML therapies will likely have to target all these LSC populations

Hematopoietic stem cell heterogeneity and age-associated platelet bias are evolutionarily conserved

Hematopoietic stem cells (HSCs) reconstitute multilineage human hematopoiesis after clinical bone marrow (BM) transplantation and are the cells of origin of some hematological malignancies. Although HSCs provide multilineage engraftment, individual murine HSCs are lineage biased and contribute unequally to blood cell lineages. Here, we performed high-throughput single-cell RNA sequencing in mice after xenograft with molecularly barcoded adult human BM HSCs. We demonstrated that human individual BM HSCs are also functionally and transcriptionally lineage biased. Specifically, we identified platelet-biased and multilineage human HSCs. Quantitative comparison of transcriptomes from single HSCs from young and aged BM showed that both the proportion of platelet-biased HSCs and their level of transcriptional platelet priming increase with age. Therefore, platelet-biased HSCs and their increased prevalence and transcriptional platelet priming during aging are conserved features of mammalian evolution

GATA1s induces hyperproliferation of eosinophil precursors in Down syndrome transient leukemia

Transient leukemia (TL) is evident in 5–10% of all neonates with Down syndrome (DS) and associated with N-terminal truncating GATA1-mutations (GATA1s). Here we report that TL cell clones generate abundant eosinophils in a substantial fraction of patients. Sorted eosinophils from patients with TL and eosinophilia carried the same GATA1s-mutation as sorted TL-blasts, consistent with their clonal origin. TL-blasts exhibited a genetic program characteristic of eosinophils and differentiated along the eosinophil lineage in vitro. Similarly, ectopic expression of Gata1s, but not Gata1, in wild-type CD34+-hematopoietic stem and progenitor cells induced hyperproliferation of eosinophil promyelocytes in vitro. While GATA1s retained the function of GATA1 to induce eosinophil genes by occupying their promoter regions, GATA1s was impaired in its ability to repress oncogenic MYC and the pro-proliferative E2F transcription network. ChIP-seq indicated reduced GATA1s occupancy at the MYC promoter. Knockdown of MYC, or the obligate E2F-cooperation partner DP1, rescued the GATA1s-induced hyperproliferative phenotype. In agreement, terminal eosinophil maturation was blocked in Gata1Δe2 knockin mice, exclusively expressing Gata1s, leading to accumulation of eosinophil precursors in blood and bone marrow. These data suggest a direct relationship between the N-terminal truncating mutations of GATA1 and clonal eosinophilia in DS patients