In our study, the midgut appeared infected during the whole incubation time.
Our comparison of midgut transcripts and brush border proteins between the susceptible and LiTOX strains revealed an overlapping but distinct set of transcripts/proteins differentially expressed.
We tested if the P. schultei cellulase and pectinase genes were endogenous in origin by mapping all genomic reads from the brain tissue back to our de novo midgut transcriptome assembly.
Our de novo midgut transcriptomes enabled us to survey all expressed PCWDEs of the Phasmatodea at once and identify conserved catalytic domains, justifying downstream translation and activity level analyses.
The AgOXT1 primers 1557F (5′-CAGCACAAGAAGCTGTTCTTTGGC-3′) and 2337R (5′-AGCTTCCGTGACGAGAAATCGTGT-3′) were used to amplify a 780 bp product corresponding to the C-terminus of AgOXT1 from our A. gambiae midgut cDNA library.
Chitin synthase gene A of the S. exigua (SeCHSA) is not expressed in the midgut, and our previous research using injection of SeCHSA dsRNA into S. exigua larvae demonstrated disruption of the larval development [20].
Our hypothesis is that midgut invasion by P. falciparum ookinetes alters mosquito gene expression at both the transcriptional and translational levels.
Yet, Dimm protein was not detected in any cells of the adult midgut under our experimental conditions, despite the fact that identical antiserum has been used to detect Dimm in other tissues (Hewes et al. 2003; Park et al. 2008).
By comparing our findings with the midgut transcriptome analyses of two other sand fly species, L. longipalpis and P. papatasi, we identified several features shared by the two permissive vectors, P. perniciosus and L. longipalpis.
For our series of metastatic midgut NENS (1989 2009), we report a 5-year OS of 61.3%, which compares with results of the Surveillance, Epidemiology and End Results (SEER) registry data (1992 1999) in which the overall 5-year survival of midgut NENs was 61%, and 50% for those with metastatic disease(Modlin et al, 2003).
