Complete mitochondrial genome of the black-winged fly, Felderimyia fuscipennis (Diptera: Tephritidae) and its phylogenetic relationship within family Tephritidae.

The black-winged fly, Felderimyia fuscipennis (Diptera: Tephritidae), is an insect pest of bamboo shoot, mainly distributed in Thailand, Malaysia and Yunnan Province and Guangxi Autonomous Region, China. The complete sequence of the mitogenome of F. fuscipennis has been determined in this study. The whole mitogenome sequence is 16,536 bp in length, which totally contains 13 protein-coding genes (PCGs), 2 rRNA genes, 22 tRNA genes, and a non-coding region (putative control region, CR). The phylogeny indicates that F. fuscipennis of subfamily Trypetinae was monophyletic and clearly separated from both Dacinae and Tephritinae with high bootstrap value supported.

Complete mitochondrial genome of melon fly, Zeugodacus cucurbitae (Diptera:Tephritidae) from Kunming, Southwest China and the phylogeny within subfamily Dacinae.

The melon fly, Zeugodacus cucurbitae (Diptera:Tephritidae) is an important invasive pest and distributed throughout tropical, subtropical countries and areas. In this study, we report the complete mitochondrial genome of the fly with 15, 685 base pair in length, which includes 37 genes (the large and small ribosomal RNA subunits, 22 transfer RNA genes, 13 genes encoding mitochondrial proteins) and a non-coding A + T-rich control region. Molecular phylogeny indicated that there was a high bootstrap value supported among Z. cucurbitae and Z. tau belonging to the Z. tau complex.

Maternal plasma concentrations of macrophage migration inhibitory factor at first trimester as a predictive biomarker of preterm delivery in Chinese women.

BACKGROUND: Infection and/or inflammation have been proposed play role in the preterm delivery (PTD) pathogenesis. Macrophage migration inhibitory factor(MIF), a mediator of innate immunity and inflammation, is induced in various infections, including those that occur during pregnancy. We assessed the relation between maternal early pregnancy plasma concentrations of MIF and PTD. METHODS: Women were recruited before 14 weeks gestation and were followed up until delivery. Maternal plasma concentrations of MIF, C-reactive protein (CRP) and interleukin 6 (IL-6) at first visit were measured by competitive immunoassay. The diagnosis of PTD was made using American College of Obstetricians and Gynaecologists (ACOG) guidelines. Logistic regression procedures were used to calculate adjusted odds ratio (OR) and 95% confidence intervals (95%CI). RESULTS: In the study period, 596 participants were included. The median plasma concentration of MIF was significantly higher in women in whom PTD later developed compared with those delivering at term (P < 0.001). For each 1 ng/ml increase of plasma concentration of MIF, the unadjusted and adjusted risk of PTD would be increased by 12% (with the OR of 1.12 [95% CI 1.07-1.17], P < 0.001) and 7% (1.07 [1.02-1.15], P = 0.002), respectively. Stratified analyses indicated that increased MIF was associated with an increased risk of spontaneous delivery (OR = 1.16, 95%CI: 1.07-1.24; P < 0.001), indicated delivery (OR = 1.05, 95%CI: 1.01-1.14; P = 0.02), and before 34 weeks' gestation delivery (OR = 1.09, 95%CI: 1.03-1.18). With an AUC of 0.71, MIF showed a significantly greater discriminatory ability as compared with BMI (0.58; 95% CI: 0.52-0.65; P < 0.001), CRP (0.61; 95% CI: 0.54-0.68; P < 0.001) and IL-6(0.63; 95% CI: 0.55-0.69; P = 0.001). CONCLUSIONS: Increased maternal plasma concentrations of MIF at first trimester were associated with increased risk of PTD and might be useful in identifying newborn at risk for PTD for early prevention strategies.

Live and dead GFP-tagged bacteria showed indistinguishable fluorescence in Caenorhabditis elegans gut.

Caenorhabditis elegans has been used for studying host-pathogen interactions since long, and many virulence genes of pathogens have been successfully identified. In several studies, fluorescent pathogens were fed to C. elegans and fluorescence observed in the gut was considered an indicator for bacterial colonization. However, the grinder in the pharynx of these nematodes supposedly crushes the bacterial cells, and the ground material is delivered to the intestine for nutrient absorption. Therefore, it remains unclear whether intact bacteria pass through the grinder and colonize in the intestine. Here we investigated whether the appearance of fluorescence is indicative of intact bacteria in the gut using both fluorescence microscopy and transmission electron microscopy. In wild-type N2 C. elegans, Escherichia coli DH5α, and Vibrio vulnificus 93U204, both of which express the green fluorescence protein, were found intact only proximal to the grinder, while crushed bacterial debris was found in the post-pharyngeal lumen. Nevertheless, the fluorescence was evident throughout the lumen of worm intestines irrespective of whether the bacteria were intact or not. We further investigated the interaction of the bacteria with C. elegans phm-2 mutant, which has a dysfunctional grinder. Both strains of bacteria were found to be intact and accumulated in the pharynx and intestine owing to the defective grinder. The fluorescence intensity of intact bacteria in phm-2 worms was indistinguishable from that of crushed bacterial debris in N2 worms. Therefore, appearance of fluorescence in the C. elegans intestine should not be directly interpreted as successful bacterial colonization in the intestine.

In vitro and in vivo wound healing-promoting activities of beta-lapachone.

Impaired wound healing is a serious problem for diabetic patients. Wound healing is a complex process that requires the cooperation of many cell types, including keratinocytes, fibroblasts, endothelial cells, and macrophages. beta-Lapachone, a natural compound extracted from the bark of the lapacho tree (Tabebuia avellanedae), is well known for its antitumor, antiinflammatory, and antineoplastic effects at different concentrations and conditions, but its effects on wound healing have not been studied. The purpose of the present study was to investigate the effects of beta-lapachone on wound healing and its underlying mechanism. In the present study, we demonstrated that a low dose of beta-lapachone enhanced the proliferation in several cells, facilitated the migration of mouse 3T3 fibroblasts and human endothelial EAhy926 cells through different MAPK signaling pathways, and accelerated scrape-wound healing in vitro. Application of ointment with or without beta-lapachone to a punched wound in normal and diabetic (db/db) mice showed that the healing process was faster in beta-lapachone-treated animals than in those treated with vehicle only. In addition, beta-lapachone induced macrophages to release VEGF and EGF, which are beneficial for growth of many cells. Our results showed that beta-lapachone can increase cell proliferation, including keratinocytes, fibroblasts, and endothelial cells, and migration of fibroblasts and endothelial cells and thus accelerate wound healing. Therefore, we suggest that beta-lapachone may have potential for therapeutic use for wound healing.