One factor limiting the success of non-viral gene therapy smooth muscle cells, we have created a series of reporter vectors is the relative inability to target genes specifically plasmids that are expressed selectively in smooth muscle to a desired cell type. To address this limitation, we have cells. Moreover, when injected into the cytoplasm, plasbegun to develop cell-specific vectors whose specificity is mids containing portions of the SMGA promoter localize to at the level of the nuclear import of the plasmid DNA. We the nucleus of smooth muscle cells, but remain cytoplashave recently shown that nuclear import of plasmid DNA mic in fibroblasts and CV1 cells. In contrast, a similar plasis a sequence-specific event, requiring the SV40 enhancer, mid carrying the SV40 enhancer is transported into the a region known to bind to a number of general transcription nuclei of all cell types tested. Nuclear import of the SMGA factors (Dean DA, Exp Cell Res 1997; 230: 293). From promoter-containing plasmids could be achieved when the these studies we developed a model whereby transcription smooth muscle specific transcription factor SRF was factor(s) bind to the DNA in the cytoplasm to create a proexpressed in stably transfected CV1 cells, supporting our tein-DNA complex that can enter the nucleus using the model for the nuclear import of plasmids. Finally, these protein import machinery. Our model predicts that by using nuclear targeting sequences were also able to promote DNA elements containing binding sites for transcription facincreased gene expression in liposome-and polycationtors expressed in unique cell types, we should be able to transfected non-dividing cells in a cell-specific manner, create plasmids that target to the nucleus in a cell-specific similar to their nuclear import activity. These results promanner. Using the promoter from the smooth muscle vide proof of principle for the development of cell-specific gamma actin (SMGA) gene whose expression is limited to non-viral vectors for any desired cell type.
The causal relationship between lactose ingestion and gastrointestinal symptoms is questionable. The aim of this study was to assess symptoms associated with milk ingestion in children with lactose maldigestion. Thirty children (11 males) age 3 to 17 years with lactose maldigestion were studied. In a double-blind, crossover design, subjects ingested 240 mL daily of either lactose-hydrolyzed or lactose-containing milk for 14 days. Diaries were kept daily that recorded diet, medication use, and symptoms. There was a significant increase in abdominal pain experienced by study participants during the lactose ingestion period when compared to the lactose-free period. We conclude that ingestion of 12 g of lactose daily is associated with increased abdominal pain in susceptible children with lactose maldigestion. A trial of dietary lactose restriction may be beneficial in reducing abdominal pain in children with lactose maldigestion.
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