Bemisia tabaci whitefly species are some of the world’s most devastating agricultural pests and plant-virus disease vectors. Elucidation of the phylogenetic relationships in the group is the basis for understanding their evolution, biogeography, gene-functions and development of novel control technologies. We report here the discovery of five new Sub-Saharan Africa (SSA) B. tabaci putative species, using the partial mitochondrial cytochrome oxidase 1 gene: SSA9, SSA10, SSA11, SSA12 and SSA13. Two of them, SSA10 and SSA11 clustered with the New World species and shared 84.8‒86.5% sequence identities. SSA10 and SSA11 provide new evidence for a close evolutionary link between the Old and New World species. Re-analysis of the evolutionary history of B. tabaci species group indicates that the new African species (SSA10 and SSA11) diverged from the New World clade c. 25 million years ago. The new putative species enable us to: (i) re-evaluate current models of B. tabaci evolution, (ii) recognise increased diversity within this cryptic species group and (iii) re-estimate divergence dates in evolutionary time.

BackgroundMesenchymal stem cells microvesicles (MSC-MVs) stabilize endothelial barrier function in acute lung injury (ALI); however, the detailed mechanism remains to be further defined. Hepatocyte growth factor (HGF), which is derived from MSC-MVs, might have a key role in the restoration of endothelial barrier function by MSC-MVs.MethodsMSCs with lentiviral vector-mediated HGF gene knockdown (siHGF-MSC) were generated. A co-culture model of pulmonary microvascular endothelial cells and MSC-MVs collected from MSCs or siHGF-MSCs after 24 h of hypoxic culture was utilized. Then, endothelial paracellular and transcellular permeabilities were detected. VE-cadherin, and occludin protein expression in the endothelial cells was measured using Western blot. Endothelial cell proliferation was analysed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium (MTT) assay. Endothelial cell apoptosis was analysed using TUNEL assay. Finally, IL-6 and IL-10 production was determined via an enzyme-linked immunosorbent assay (ELISA).ResultsTreatment with MSC-MVs significantly decreased LPS-induced endothelial paracellular and transcellular permeabilities, and the effect was significantly inhibited after HGF gene knockdown in MSC-MVs. Furthermore, treatment with MSC-MVs increased the expression of the endothelial intercellular junction proteins VE-cadherin and occludin. Treatment with MSC-MVs also decreased endothelial apoptosis and induced endothelial cell proliferation. Finally, the treatment reduced IL-6 production and increased IL-10 production in the conditioned media of endothelial cells. However, the effects of the treatment with MSC-MVs were inhibited after HGF gene knockdown.ConclusionsMSC-MVs protect the barrier functions of pulmonary microvascular endothelial cells, which can be partly attributed to the presence of HGF in the MSC-MVs.

BackgroundThe whiteflies under the name Bemisia tabaci (Gennadius) (Aleyrodidae: Hemiptera) are species complex of at least 31 cryptic species some of which are globally invasive agricultural pests. Previously, the mitochondrial genome (mitogenome) of the indigenous New World B. tabaci species was sequenced and major differences of gene order from the postulated whitefly ancestral gene order were found. However, the sequence and gene order of mitogenomes in other B. tabaci species are unknown. In addition, the sequence divergences and gene expression profiles of mitogenomes in the B. tabaci species complex remain completely unexplored.ResultsIn this study, we obtained the complete mitogenome (15,632 bp) of the invasive Mediterranean (MED), which has been identified as the type species of the B. tabaci complex. It encodes 37 genes, including 13 protein-coding genes (PCGs), 2 ribosomal RNAs and 22 transfer RNAs (tRNA). Comparative analyses of the mitogenomes from MED and New World (previously published) species reveal that there are no gene arrangements. Based on the Illumina sequencing data, the gene expression profile of the MED mitogenome was analyzed. We found that a number of genes were polyadenylated and the partial stop codons in cox1, cox2 and nd5 are completed via polyadenylation that changed T to the TAA stop codon. In addition, combining the transcriptome with the sequence alignment data, the possible termination site of some PCGs were defined. Our analyses also revealed that atp6 and atp8, nd4 and nd4l, nd6 and cytb were found on the same cistronic transcripts, whereas the other mature mitochondrial transcripts were monocistronic. Furthermore, RT-PCR analyses of the mitochondrial PCGs expression in different developmental stages revealed that the expression level of individual mitochondrial genes varied in each developmental stage of nymph, pupa and adult. Interestingly, mRNA levels showed significant differences among genes located in the same transcription unit suggesting that mitochondrial mRNA abundance is heavily modulated by post-transcriptional regulation.ConclusionsThis work provides novel insights into the mitogenome evolution of B. tabaci species and demonstrates that utilizing RNA-seq data to obtain the mitogenome and analyze mitochondrial gene expression characteristics is practical.

IntroductionGlutamine supplementation is supposed to reduce mortality and nosocomial infections in critically ill patients. However, the recently published reducing deaths due to oxidative stress (REDOX) trials did not provide evidence supporting this. This study investigated the impact of glutamine-supplemented nutrition on the outcomes of critically ill patients using a meta-analysis.MethodsWe searched for and gathered data from the Cochrane Central Register of Controlled Trials, MEDLINE, Elsevier, Web of Science and ClinicalTrials.gov databases reporting the effects of glutamine supplementation on outcomes in critically ill patients. We produced subgroup analyses of the trials according to specific patient populations, modes of nutrition and glutamine dosages.ResultsAmong 823 related articles, eighteen Randomized Controlled Trials (RCTs) met all inclusion criteria. Mortality events among 3,383 patients were reported in 17 RCTs. Mortality showed no significant difference between glutamine group and control group. In the high dosage subgroup (above 0.5 g/kg/d), the mortality rate in the glutamine group was significantly higher than that of the control group (relative risk (RR) 1.18; 95% confidence interval (CI), 1.02 to 1.38; P = 0.03). In 15 trials, which included a total of 2,862 patients, glutamine supplementation reportedly affected the incidence of nosocomial infections in the critically ill patients observed. The incidence of nosocomial infections in the glutamine group was significantly lower than that of the control group (RR 0.85; 95% CI, 0.74 to 0.97; P = 0.02). In the surgical ICU subgroup, glutamine supplementation statistically reduced the rate of nosocomial infections (RR 0.70; 95% CI, 0.52 to 0.94; P = 0.04). In the parental nutrition subgroup, glutamine supplementation statistically reduced the rate of nosocomial infections (RR 0.83; 95% CI, 0.70 to 0.98; P = 0.03). The length of hospital stay was reported in 14 trials, in which a total of 2,777 patients were enrolled; however, the patient length of stay was not affected by glutamine supplementation.ConclusionsGlutamine supplementation conferred no overall mortality and length of hospital stay benefit in critically ill patients. However, this therapy reduced nosocomial infections among critically ill patients, which differed according to patient populations, modes of nutrition and glutamine dosages.