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Babesiosis is a malaria-like disease in humans and animals that is caused by Babesia species, which are tick-transmitted apicomplexan pathogens. Babesia duncani causes severe to lethal infection in humans, but despite the risk that this parasite poses as an emerging pathogen, little is known about its biology, metabolic requirements or pathogenesis. Unlike other apicomplexan parasites that infect red blood cells, B. duncani can be continuously cultured in vitro in human erythrocytes and can infect mice resulting in fulminant babesiosis and death. We report comprehensive, detailed molecular, genomic, transcriptomic and epigenetic analyses to gain insights into the biology of B. duncani. We completed the assembly, 3D structure and annotation of its nuclear genome, and analysed its transcriptomic and epigenetics profiles during its asexual life cycle stages in human erythrocytes. We used RNA-seq data to produce an atlas of parasite metabolism during its intraerythrocytic life cycle. Characterization of the B. duncani genome, epigenome and transcriptome identified classes of candidate virulence factors, antigens for diagnosis of active infection and several attractive drug targets. Furthermore, metabolic reconstitutions from genome annotation and in vitro efficacy studies identified antifolates, pyrimethamine and WR-99210 as potent inhibitors of B. duncani to establish a pipeline of small molecules that could be developed as effective therapies for the treatment of human babesiosis.

Simple Summary: Zinc is an essential mineral element for broiler growth and development. In the present study, we found that dietary Zn deficiency decreased the number of proliferating cell nuclear antigen-positive cells and inhibited PI3K, AKT, and mTOR phosphorylation along with the downregulation of GPR39 protein expression in the jejunum of broiler on d 42. These findings suggest that dietary Zn deficiency inhibits cell proliferation possibly via the GPR39-mediated suppression of the PI3K/AKT/mTOR signaling pathway in the jejunum of broilers. A prior investigation revealed that a lack of Zinc (Zn) could hinder intestinal cell proliferation in broiler chickens; however, the mechanisms responsible for this effect remain unclear. We aimed to investigate the possible mechanisms of dietary Zn deficiency in inhibiting the jejunal cell proliferation of broilers. For this study, a total of 112 chickens (21 days old) were randomly divided into two treatments (seven replicate cages per treatment, eight chickens per replicate cage): the control group (CON) and the Zn deficiency group. The duration of feeding was 21 d. Chickens in the control group were provided with a basal diet containing an extra addition of 40 mg Zn/kg in the form of Zn sulfate, whereas chickens in the Zn deficiency group were given the basal diet with no Zn supplementation. The results indicated that, in comparison to the CON, Zn deficiency increased (p < 0.05) the duodenal and jejunal crypt depth (CD) of broilers on d 28 and jejunal and ileal CD on d 35, and decreased (p < 0.05) the duodenal, jejunal, and ileal villus height/crypt depth (VH/CD) on d 28 and the jejunal VH, jejunal and ileal villus surface area, and VH/CD on d 35. Furthermore, Zn deficiency decreased (p < 0.0001) the number of proliferating cell nuclear antigen-positive cells and downregulated (p < 0.01) the mRNA or protein expression levels of phosphatidylinositol 3-kinase (PI3K), phosphorylated PI3K, phosphorylated serine–threonine kinase (AKT), phosphorylated mechanistic target of rapamycin (mTOR), G protein-coupled receptor 39 (GPR39), and extracellular-regulated protein kinase, but upregulated (p < 0.05) the mRNA or protein expression levels of P38 mitogen-activated protein kinase, c-jun N-terminal kinase (JNK) 1 and JNK2, and phosphorylated protein kinase C in the jejunum of the broilers on d 42. It was concluded that dietary Zn deficiency inhibited cell proliferation possibly via the GPR39-mediated suppression of the PI3K/AKT/mTOR signaling pathway in the jejunum of broilers. [ABSTRACT FROM AUTHOR]

[Objectives] The elbow is a common component of ship piping system. Efforts have been made in order to predict the elbow erosion accurately.[Methods] In this paper,the numerical simulation is conducted to calculate and analyze the flow field inside the pipe. From the two aspects,i.e. the influence of the turbulence model on the prediction of the flow field in the elbow and the influence of turbulence model on elbow erosion calculation,intensive research into the method to predict the erosion of elbow by solid and liquid flows.[Results] The results show that the SST k-ω turbulence model,together with the Oka erosion model,can accurately predict the flow field distribution in the elbow. Turbulence model brings a significant impact on the abrasion calculation,where it affects the calculated value of final erosion and also makes a great difference in the distribution of predicted relative erosion.[Conclusions] The obtained results can provide guidance for future pipe erosion prediction.

We have investigated the electronic and transport properties of a series of 2D Fc(X)n–MoS2 (Fc=Fe(Cp)2; X=SiH2, CH2, CH=CH, or C≡C; n = 1 or 2) systems by using ferrocene derivatives Fc(X)n to be grafted onto a MoS2 surface. Calculations have been carried out by density functional theory (DFT) and nonequilibrium Green's function (NEGF) methods. All these Fc(X)n–MoS2 give type-II heterostructures, and the grafted Fc(X)n behaves as a quantum dot-like group. No matter which Fc(X)n group is introduced, the conductivity is improved. The current magnitudes at a certain bias voltage follow the sequence of Fc(C≡C)-MoS2 ≈ Fc(CH=CH)-MoS2 > Fc(SiH2)2-MoS2 ≈ Fc(SiH2)-MoS2 > Fc(CH2)2-MoS2 ≈ Fc(CH2)-MoS2, corresponding well to the abilities of supplying electrons from the (X)n group to MoS2. The armchair direction exhibits a larger current by about 4 times compared to the zigzag direction. A distinct NDR behavior is found for the Fc(C≡C)-MoS2, meaning that the transport channel can be electrically switched from the off state to the on state, and again turned to the off state. [ABSTRACT FROM AUTHOR]