Phage lambda integration protein: synthesis in lambda-infected minicells and membrane affinity.
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Biomedical subjects
Publications and source records attributed to K Taylor.
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The authors describe an unusual form of pancreatic necrosis in which the excavated necrotic core is surrounded by a shell of tissue and forms a sac which generally conforms to the axis and contour of the pancreas. This debris-containing sac could be misinterpreted on ultrasound and CT and is best defined by direct injection into the pancreatic duct.
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When a family member is hospitalized, family dynamics change. One hospital seeks to help a family better cope with one member's illness through educational programs and hospital policies that seek to strengthen the family unit and to involve the family in patient care.
Phage lambda major head protein, the gene E product, has been identified among other phage proteins synthesized in lambda-infected Escherichia coli minicells, separated by SDS-acrylamide gel electrophoresis. On stained gels, the same protein has also been detected among total (bacterial and phage) proteins of lambda-infected minicells. The contribution of lambda proteins to the total protein content of lambda-infected minicells was found to be about 12% following 30 min lambda-infection. The inhibition of lambda early protein synthesis (shown by other authors in nucleate bacterial cells) practically does not occur in minicells; this may be the reason of the observed high efficiency of phage protein synthesis.
A variable population of fat-filled "foam" cells in diet-induced experimental arterial intimal plaques of rabbits and monkeys were analyzed for several features characteristic of macrophages. These included: 1) surface binding and phagocytosis of antibody-coated or complement-coated erythrocytes to detect specific surface receptors; 2) cytochemical tests and ultrastructural features to evaluate cell function and structure; and 3) rapid adherence to glass, a feature of macrophage activity, to isolate and identify a homogeneous population of fat-filled foam cells from excised and disrupted arterial lesions. Mixed populations of cells grown in culture from explants of lesions were also analyzed and lipid-filled cells were studied in histologic sections of adjacent lesions. Eighty to ninety percent of the easily dislodged glass-adherent cells from lesions had surface receptors for the Fc portion of immunoglobulin G and for the third component of complement. Coated red blood cells were readily phagocytized, but noncoated cells were not. Acid lipase activity was demonstrated in the Fc-receptor-positive cells. These cells were also devoid of ultrastructural features of smooth muscle. Among the cells growing or migrating out of explants, a population of large round foam cells possessed all of the macrophage features found in the glass-adherent cells from lesions and lacked ultrastructural characteristics of smooth muscle. Fusiform lipid vacuolated cells also grew out of the explants but did not exhibit surface receptors, failed to phagocytize coated or noncoated erythrocytes and did not stain for acid lipase activity; these cells showed distinctive morphologic features of smooth muscle. In histologic sections of nearby lesions foam cells that showed macrophage characteristics, ie, acid lipase activity and the presence of lysozymelike antigen, lacked ultrastructural smooth muscle features. Smooth muscle cells in lesion sections often contained lipid but demonstrated no lysozyme or acid lipase activity. The occurrence of a population of cells with several functional and structural features of macrophages among the lipid-laden cells of experimental diet-induced arterial lesions suggests that some foam cells may be derived from monocytes. An alternative explanation, that metabolically altered autochthonous arterial wall cells assume one or more characteristics of mononuclear phagocytes is less likely, since some of the markers used in these experiments are unrelated. Both explanations deserve further careful study.
In this study, we have evaluated one aspect of the cellular immune process--in vitro release of MIF by lymphocytes obtained from controls; well-controlled, ketosis-prone, insulin-dependent diabetic patients; nonketotic diabetic patients; and nonhyperglycemic obese patients. The results showed that MIF release by cells from well-controlled, insulin-dependent diabetic, nonketotic diabetic, and nonhyperglycemic obese subjects was 100% +/- 8, 48% +/- 17, and 36% +/- 17 of control values, respectively. Thus insulin-sensitive, ketosis-prone diabetic patients have normal MIf release while well-controlled on insulin therapy, whereas insulin-resistant, nonketotic diabetic and nonhyperglycemic obese patients have impaired MIF release. It is possible that this in vitro defect in a cellular immune process is related to the insulin-resistant state and that it may play a role in enhanced susceptibility to infection in insulin-resistant diabetic patients.
The present case represents, to our knowledge, the longest period of oliguric renal failure after renal transplant with eventual recovery reported to date. The disparity between the renogram and the eventual results of renal biopsy specimen examination highlights the difficulty in managing such patients. The renal biopsy specimen in such patients may provide not only diagnostic information, but also may have direct bearing on contemplated alterations in drug regimens.
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The fate of phage lambda DNA in lambda-infected Escherichia coli minicells harboring the plasmid ColE1, and in plasmid-free minicells, were studied. Binding of lambda DNA to the minicell membrane, and formation of the supercoiled covalently-closed circular structure has been demonstrated. Phage infection abolishes plasmid DNA synthesis. Only a very slight, non-replicative lambda DNA synthesis occurs, soon after infection. This synthesis is associated with fragments of lambda DNA arising during, or soon after its penetration.
Clearance experiments were performed in the rat to examine the effects of diuretics on the renal transport of oxalate. In addition, the effect of infusing either uric acid or calcium on the renal transport of oxalate was examined. During control periods, the fractional excretion of oxalate (FEOx) averaged 118.0 +/- 2.1%. Acute administration of either chlorothiazide, furosemide, or indanyl-oxyacetic acid (MK-196), a new uricosuric diuretic, resulted in a significant decrease in the FEOx in all groups to 104.8 +/- 2.4%, 111.3 +/- 2.1%, and 108.6 +/- 2.7%, respectively. Infusion of uric acid increased urinary uric acid excretion from 2.41 +/- 0.28 to 4.26 +/- 0.03 micrograms/min/g kidney wt (P less than 0.001) and decreased FEOx to 104.0 +/- 2.4% (P less than 0.001 compared to control). Infusion of calcium chloride increased urinary calcium excretion from 0.10 +/- 0.04 to 0.44 +/- 0.06 micrograms/min/g kidney wt (P less than 0.001) but had no effect on the FEOx which averaged 118.3 +/- 8.3% (P = NS compared to control). These studies show that the acute administration of chlorothiazide, furosemide, or MK-196, as well as increasing urinary uric acid excretion by uric acid infusion, are all associated with a decrease in the FEOx. Acutely increasing urinary calcium excretion, however, had no effect on oxalate transport.
Glomerulonephritis induced by antibodies to the glomerular basement membrane is a well recognized cause of renal disease and is responsible for 5% to 15% of all glomerular disease. The patients usually present with an acute nephritic syndrome followed by rapidly progressive renal failure. We report two patients who presented with the nephrotic syndrome and anti-GBM glomerulonephritis, and who exhibited differing clinical courses not characteristic of "rapidly progressive glomerulonephritis" or Goodpasture's syndrome.
We have proved by acrylamide gel electrophoresis that DNA-free ghosts of bacteriophage lambda obtained by osmotic shock (S-ghosts), or by incubation in 5 M-L-Cl (L-ghosts) do not possess the proteins specified by the genes J and H. Electron microscopy of L-ghosts showed that they are devoid of the whole tail tip, composed of the basal part and the tail fibre. The lack of the J-gene product, which is believed to be the tail fibre, explains why S- and L-ghosts do not adsorb to susceptible bacteria. Our results suggest that the H-gene product, which is modified after translation, is situated in the basal part of the tail.
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The effects of ticrynafen, a uricosuric diuretic, were examined utilizing free-flow micropuncture and clearance techniques in the rat. The intravenous infusion of ticrynafen (50 mg/kg body wt/hr) had no effect on glomerular filtration rate, but resulted in significant increases in urine flow from 4.4 +/- 0.7 microliter/min/g kidney wt to 19.2 +/- 2.6 (p less than 0.001); in urinary sodium excretion from 0.14 +/- 0.07 micronEq/min/g kidney wt to 2.35 +/- 0.52 (p less than 0.01); and in urinary urate excretion from 2.8 +/- 0.2 microgram/min/g kidney wt to 4.0 +/- 0.2 (p less than 0.005). There was no change in urinary phosphate excretion. The end-proximal TF/Pinulin ratio was 2.66 +/- 0.18 in control and 2.67 +/- 0.16 in experimental periods (p=NS). In awake animals, ticrynafen administration resulted in a decrease in CH2O from 6.47 +/- 0.12% to 3.50 +/- 0.69 (p less than 0.05), but no change in TCH2O. These studies demonstrate that ticrynafen is a uricosuric and diuretic agent in the rat. The natriuresis appears to derive from an inhibitory action of this agent in the cortical diluting segment of the nephron. In comparison to a related uricosuric diuretic, MK-196, ticrynafen is a less potent agent with respect to both its uricosuric and diuretic properties in the rat.
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