The arms race between entomopathogenic bacteria and their insect hosts is an excellent model for decoding the intricate coevolutionary processes of host-pathogen interaction. Here, we demonstrate that the MAPK signaling pathway is a general switch to trans-regulate differential expression of aminopeptidase N and other midgut genes in an insect host, diamondback moth (Plutella xylostella), thereby countering the virulence effect of Bacillus thuringiensis (Bt) toxins. Moreover, the MAPK cascade is activated and fine-tuned by the crosstalk between two major insect hormones, 20-hydroxyecdysone (20E) and juvenile hormone (JH) to elicit an important physiological response (i.e. Bt resistance) without incurring the significant fitness costs often associated with pathogen resistance. Hormones are well known to orchestrate physiological trade-offs in a wide variety of organisms, and our work decodes a hitherto undescribed function of these classic hormones and suggests that hormonal signaling plasticity is a general cross-kingdom strategy to fend off pathogens.

Fructose-bisphosphate aldolase A (ALDOA) is a key enzyme in glycolysis and is responsible for catalyzing the reversible conversion of fructose-1,6-bisphosphate to glyceraldehydes-3-phosphate and dihydroxyacetone phosphate. ALDOA contributes to various cellular functions such as muscle maintenance, regulation of cell shape and mobility, striated muscle contraction, actin filament organization and ATP biosynthetic process. Here, we reported that ALDOA is a highly expressed in lung squamous cell carcinoma (LSCC) and its expression level is correlated with LSCC metastasis, grades, differentiation status and poor prognosis. Depletion of ALDOA expression in the lung squamous carcinoma NCI-H520 cells reduces the capabilities of cell motility and tumorigenesis. These data suggest that ALDOA could be a potential marker for LSCC metastasis and a therapeutic target for drug development.

BACKGROUND/OBJECTIVES: Lipid accumulation product (LAP) is an index, which combines waist circumference (WC) and triglyceride (TG) reflecting lipid accumulation. The aims of the study were to explore the relationship between LAP and insulin resistance (IR) and to assess whether LAP was superior to WC and body mass index (BMI) in identifying IR. SUBJECTS/METHODS: The study was cross-sectional and included 2524 non-diabetic subjects from China. The blood pressure (BP), anthropometric measurements, glucose levels, insulin levels and a fasting lipid profile were measured. BMI, the homeostasis model assessment of IR (HOMA-IR) and LAP were calculated. RESULTS: In both sexes, BP, BMI, total cholesterol (TC), non high-density lipoprotein cholesterol (non-HDL-C), HOMA-IR, fasting and postprandial glucose levels increased across LAP quartiles (Po0.001), while HDL cholesterol (HDL-C) levels decreased across LAP quartiles (Po0.001). Pearson's correlation analysis demonstrated that HOMA-IR was correlated with LAP, BMI, WC, TG, HDL-C and non-HDL-C in both sexes (Po0.001). Multivariate analysis demonstrated that LAP had a greater impact on HOMA-IR than BMI and WC. CONCLUSIONS: LAP is closely associated with HOMA-IR and is a powerful index that outperforms BMI and WC in identifying IR in non-diabetic individuals.

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