Crown gall disease results from the insertion of a segment of the Agrobacterium Ti plasmid, called T-DNA, into host plant nuclear DNA. We have subjected to sequence analysis the border regions of pTi T37 (ends of T-DNA) and one left T-DNA/plant DNA border fragment isolated from BT37 tobacco teratoma by molecular cloning. These sequence studies, taken together with published sequence of a right T-DNA/plant DNA border fragment, allowed us to identify the positions of left and right borders at the DNA sequence level. Comparison of left and right border regions of the Ti plasmid revealed a "core" direct repeat of 13 of 14 bases (12 contiguous) precisely at the borders of T-DNA. An extended repeat of 21 of 25 bases overlaps this core repeat. T-DNA on the Ti plasmid exhibits no longer direct or inverted repeats in the border regions, based on Southern hybridization studies. The physical structure of T-DNA differs from that of known prokaryotic and eukaryotic transposable elements but bears a structural resemblance to the prophage of bacteriophage A.in the center of T-DNA (29). In contrast to the complex T-DNA inserts found in the octopine tumors, T-DNA of the nopaline tumors has a more simple arrangement. It appears colinear with T-DNA of the Ti plasmid, with borders that appear fixed, within the resolution of the technique of Southern blot analysis. The host plant DNA sites at which it inserts appear to be variable (17). In addition, T-DNA in nopaline tumors includes "fusion" DNA fragments homologous to the left and right edges of T-DNA, presumed to derive from either tandem copies or circular forms of T-DNA (30).If T-DNA is a discrete physical and genetic element, the DNA sequences at its edges might structurally define it. We have subjected to sequence analysis DNA from regions of the nopaline Ti plasmid pTi T37 that contain the left and right edges of T-DNA. The flanking Ti plasmid DNA exhibits short direct repeats that we propose to be border signals.Crown gall is a neoplastic disease of higher plants caused by oncogenic strains of Agrobacterium tumefaciens (1). Tumor cells are stably transformed in that they exhibit hormone autotrophy in vitro in the absence of the inciting bacterium (2). Axenic tumor cells synthesize one or more novel metabolites called opines (3-7) that are specific catabolic substrates for the inciting Agrobacterium strain (5, 7-9). The pathogen harbors large plasmids called Ti (tumor inducing) plasmids (10) that code for oncogenicity and specify which opines the tumor will synthesize as well as which opines the bacteria can catabolize (8,9,11,12). A part of the Ti plasmid called T-DNA is stably maintained in the tumor cells (13)(14)(15)(16)(17) and is transcribed into polyadenylylated RNAs (14,(18)(19)(20). T-DNA transcripts are found on polysomes in the tumor cell (20) and can be translated into proteins in vitro (21). Insertion of transposons into the T-DNA region of the Ti plasmid can affect tumor morphology (22-24) or eliminate the synthesis of opines by the tumor (24, 25). T-DN...
Glycogen deposition in vascular smooth muscle has been demonstrated previously in alpha-glucosidase deficiency but has not been clinically significant. Three sons of healthy, nonconsanguineous parents developed progressive proximal muscular weakness secondary to alpha-glucosidase deficiency. Each patient developed a fusiform basilar artery aneurysm, which was complicated by fatal rupture in two patients and a cerebellar infarction in the third. Postmortem examination demonstrated severe vacuolation of skeletal muscle, liver, and vascular smooth muscle with accumulation of periodic acid-Schiff-positive, diastase-sensitive material. In the surviving brother, similar glycogen deposition was demonstrated in the smooth muscle of the superficial temporal artery. Basilar artery aneurysm formation in this sibship may be a consequence of alpha-glucosidase deficiency.
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In the present review, we summarize the principles governing the transport of fluid and electrolytes across the peritoneum during continuous ambulatory peritoneal dialysis (CAPD) in "average" patients and during ultrafiltration failure (UFF), according to the three-pore model of peritoneal transport. The UF volume curves as a function of dwell time [V(t)] are determined in their early phase by the glucose osmotic conductance [product of the UF coefficient (L p S) and the glucose reflection coefficient (σ σ σ σ σ g )] of the peritoneum; in their middle portion by intraperitoneal volume and glucose diffusivity; and in their late portion by the L p S, Starling forces, and lymph flow. The most common cause of UFF is increased transport of small solutes (glucose) across the peritoneum, whereas the L p S is only moderately affected. Concerning peritoneal ion transport, ions that are already more or less fully equilibrated across the membrane at the start of the dwell, such as Na + (Cl -), Ca 2+ , and Mg 2+ , have a convection-dominated transport. The removal of these ions is proportional to UF volume (approximately 10 mmol/L Na + and 0.12 mmol/L Ca 2+ removed per deciliter UF in 4 hours). The present article examines the impact on fluid and solute transport of varying concentrations of Ca 2+ and Na + in peritoneal dialysis solutions. Particularly, the effect of "ultralow" sodium solutions on transport and UF is simulated and discussed. Ions with high initial concentration gradients across the peritoneum, such as K + , phosphate, and bicarbonate, display a diffusion-dominated transport. The transport of these ions can be adequately described by non-electrolyte equations. However, for ions that are in (or near) their diffusion equilibrium over the peritoneum (Na + , Ca 2+ , Mg 2+ ), more complex ion transport equations need to be used. Due to the complexity of these equations, however, non-electrolyte transport formalism is commonly employed, which leads to a marked underestimation of mass transfer area coefficients (PS). This can be avoided by determining the PS when transperitoneal ion concentration gradients are steep. Perit Dial Int 2004; 24:10-27 www.PDIConnect.com
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