Although the reason for this association remains unclear, this finding may suggest that the timing of GI onset relative to autism is an important variable to consider in the design of future prospective studies investigating the microbiota of children with autism. Although we found only a trend for increased Firmicutes in AUT-GI children, the cumulative levels of Firmicutes and Proteobacteria were significantly higher. In addition, the AUT-GI group had elevated levels of Betaproteobacteria compared to the Control-GI group, primarily reflecting the presence of Alcaligenaceae. Lomitapide Mesylate Alcaligenaceae sequences were not detected in any tissues from Control-GI children. Deficient digestion and absorption of monosaccharides in the small intestine may alter the balance of growth substrates, thus eliminating the growth advantages that Bacteroidetes enjoy in the healthy intestine and enabling competitive growth of bacterial phylotypes better suited for growth on undigested and unabsorbed carbohydrates. In support of this hypothesis, multiple linear regression models demonstrated that levels of ileal SGLT1 and SI mRNA were associated with levels of Bacteroidetes in ileum and cecum, or cecum alone, respectively. Levels of ileal SI, MGAM, and GLUT2 mRNA were associated with levels of cecal Firmicutes, although the magnitude of the effects of MGAM and GLUT2 differed between AUT-GI and Control-GI children. By transiently altering tumor blood vessel physiology during systemic anti-cancer treatment, tissue perfusion and drainage can be enhanced, thereby relieving interstitial hypertension. Prolonged treatment with anti-angiogenic drugs, such as Sunitinib or DC101, normalizes blood flow through the remaining stabilized vasculature. These treatments can improve tumor micro-hemodynamics and effectively lower the interstitial pressure. Consequently, the efficacy of concomitantly or subsequently Sarafloxacin HCl administered drugs is enhanced due to improved vascular delivery. Similarly, treatment of hepatic tumors with interferon-b induces tumor vessel maturation and tissue perfusion, which improves delivery of additional therapeutics. Altering oncogenic signaling in tumors can also be used to change their blood-flow dynamics.