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  • 1
    Electronic Resource
    Electronic Resource
    AUGMENTED HISTAMINE TEST (1967)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 140 (1967), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Notes: (1) The value of and the applications for the augmented histamine test are discussed. Proposals are put forth in reference to the nomenclature of gastric acid and the interpretation of the augmented histamine test for routine clinical purposes.(2) The results of the augmented histamine test in 14 patients with proven gastric ulcer and in 68 subjects with proven duodenal ulcer are presented. The mean acid outputs of men with gastric ulcer (all sites) for basal and histamine-stimulated secretion were about one-half that of men with duodenal ulcer. These differences were significant, statistically.(3) Duodenal ulcer patients with complications had a significantly higher maximal acid output to histamine than those without complication. The finding of a maximal acid output greater than 40 mEq/hr is highly suggestive of the presence or the imminence of a complication.(4) We prefer the use of the augmented histamine test as a routine gastric analysis procedure, since it is a quantitative test and, as such, gives reproducible acid output in the same individual, provides an estimate of the parietal cell mass, and gives a positive lead to the diagnosis of Zollinger-Ellison syndrome.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1967.tb51010.x
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  • 2
    Electronic Resource
    Electronic Resource
    Iron complexes of thioacroleins derived from thietes (1973)
    s.l. : American Chemical Society
    Journal of the American Chemical Society 95 (1973), S. 6113-6114 
    Details
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ja00799a046
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  • 3
    Electronic Resource
    Electronic Resource
    An ultrastructural study of sympathetic ganglion satellite cells in the rat 1. Normal and x-ray irradiated satellite cells (1973)
    Springer
    Journal of neural transmission 34 (1973), S. 215-234 
    Details
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The ultrastructure of normal and irradiated satellite cells of the rat superior cervical ganglia was studied. Each neuron is closely and completely invested by satellite cell cytoplasm. The satellite cell cytoplasm usually contains a number of mitochondria, granular endoplasmic reticulum, Golgi apparatus, lysosome-like bodies, filaments, microtubules, lipid droplets, centriole and cilia. The satellite cell also encloses presynaptic nerve endings, and other nerve fibers. X-ray irradiation produces several changes in the satellite cells. These include: (a) increased nuclear density, (b) marked local widening of the perinuclear space, (c) dilation of granular endoplasmic reticulum and loss of attached ribosomes, (d) swelling of mitochondria with disorganization of mitochondrial cristae and loss of matrix, (e) increase in the number of vacuoles, and (f) increase in the number, size and contents of lysosome-like bodies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01367511
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  • 4
    Electronic Resource
    Electronic Resource
    Improvement of health outcomes after continued implementation of a clinical pathway for radical nephrectomy (2000)
    Springer
    World journal of urology 18 (2000), S. 417-421 
    Details
    ISSN: 1433-8726
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The clinical pathway is an important tool for outcome management. We evaluated the overall effects of the continued implementation of a clinical pathway for radical nephrectomy on the length of hospital stay, admission charges, and the quality of medical care. The data obtained from the second-year implementation (group 3) of the clinical pathway were compared with the data from the first-year implementation (group 2) and the year preceding implementation (group 1). Thirty-seven consecutive patients with renal cell carcinoma underwent radical nephrectomy in group 1, 47 in group 2, and 55 in group 3; all were enrolled in this study. The length of hospital stay, average admission charges, and 8 quality indicators were measured in these patients. We also evaluated the variances in the implementation of the clinical pathway. The mean length of stay decreased by 14.0% (P=0.0048) in group 2, and by 15.8% (P=0.0014) in group 3, when compared to group 1. The total admission charges significantly decreased by 19.0% (P=0.001) in group 2, and by 27.9% (P 〈 0.0001) in group 3, compared to the charges for group 1. A continued decrease in charges for operation and anesthesia, laboratory, pharmacy, and others were found 2 years after implementation of the clinical pathway. Among the 8 quality indicators, 2 were continuously improved in the second-year implementation of the clinical pathway, 2 were improved significantly in the second-year implementation only, and 4 showed no significant change at all. Variances from the clinical pathway decreased significantly after continued implementation. Continued implementation of the clinical pathway for radical nephrectomy can improve a physician's practice continuously by decreasing the length of hospital stay, admission charges, and variances, and by improving quality. However, the improved results after implementation of the clinical pathway should be maintained carefully to assure good health care.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003450000158
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  • 5
    Electronic Resource
    Electronic Resource
    Evolutionary origins of two tightly linked mutations in arylsulfatase-A pseudodeficiency (1997)
    Springer
    Human genetics 〈Berlin〉 101 (1997), S. 135-140 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Deficient arylsulfatase A activity causes the neurodegenerative disease metachromatic leukodystrophy. However, some individuals with deficient enzyme activity appear clinically normal. This “pseudodeficiency” allele commonly found among many reported populations (frequency ∼ 0.10) is associated with two A→G transitions in cis in the arylsulfatase A gene causing the simultaneous loss of an N-glycosylation and a polyadenylation signal. To understand the evolutionary relationship between such common and tightly linked mutations, we studied 400 individuals in the African, European, Indian and East Asian populations and found none carrying the polyadenylation mutation alone. However, the N-glycosylation mutation could occur independently. Its frequency varied from 0.01 in Indians, 0.06 in Europeans, 0.21 in East Asians to 0.32 in Africans. The frequencies of both mutations occurring together ranged from almost non-existent in the Africans and East Asians, to 0.075 in the Europeans and 0.125 in the Indians. These frequencies were significantly different among populations. Haplotype analysis among homozygous pseudodeficiency individuals and eight multi-generation families with six polymorphic enzymes showed that, of the five haplotypes found in the general population, only one was linked to the double mutations. Alleles among the four populations with only the N-glycosylation mutation also supported linkage to the same haplotype except in some Europeans whose alleles were discordant. These results are consistent with the hypothesis that the N-glycosylation mutation may be a recurrent event among the Europeans but first occurred in an ancestral allele before the emergence of modern Homo sapiens from Africa at ∼100 000–200 000 years ago. Subsequently, the polyadenylation mutation occurred in this ancient allele with the N-glycosylation mutation, an event that likely took place after the divergence between the European and East Asian lineages.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004390050602
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  • 6
    Electronic Resource
    Electronic Resource
    Deficient glycosylation of arylsulfatase A in pseudo arylsulfatase-A deficiency (1990)
    Springer
    Molecular and cellular biochemistry 92 (1990), S. 117-127 
    Details
    ISSN: 1573-4919
    Keywords: lysosomal storage disease ; metachromatic leukodystrophy ; beta-Hexosaminidase ; targeting to lysosomes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Summary Deficient arylsulfatase-A activity is diagnostic of a neurodegenerative human lysosomal storage disease, metachromatic leukodystrophy. Paradoxically, similar enzyme deficiency also occurs in normal individuals, who are known as being pseudo arylsulfatase-A deficient. We showed previously that this phenotype is associated with a structural gene mutation that produces an exceptionally labile enzyme. We now report on the nature and consequence of this mutation. When the mutant arylsulfatase-A is deglycosylated by endoglycosidase H, only one smaller molecular species was generated, instead of the two from the normal enzyme. This is consistent with the loss of one of the two N-linked oligosaccharide side chains known to be present on the wild-type enzyme. Quantitative analysis of mannose and leucine incorporation showed that the mutant enzyme incorporated two- to tenfold less mannose than the normal enzyme on a molar basis. This deficient glycosylation was specific to arylsulfatase-A. Another lysosomal enzyme not affected in this mutation, beta-hexosaminidase, was glycosylated normally in the mutant cells. The remaining single oligosaccharide side chain released from the mutant arylsulfatase-A by pronase digestion was normally processed to complex and high-mannose forms. However, the high-mannose side chains contained 30% fewer phosphorylated residues than those of the normal enzyme. Nevertheless, this reduced level of phosphorylation did not prevent targeting of the mutant enzyme to the lysosomes, a process normally mediated through phosphorylated mannose residues. In conclusion, pseudo arylsulfatase-A deficiency is a unique human mutation associated with reduced glycosylation and phosphorylation of a lysosomal enzyme with the loss of one of the two carbohydrate side chains. The mutation results in greatly reduced enzyme stability, thus indicating a role for oligosaccharides in maintaining enzyme stability within the degradative environment of the lysosomes. However, the residual catalytic activity or subcellular targeting of the mutant enzyme was not affected. These properties probably account for the benign clinical presentation of pseudo arylsulfatase-A deficiency.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00218129
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  • 7
    Electronic Resource
    Electronic Resource
    Biochemical variability of arylsulphatases-A,-B and-C in cultured fibroblasts from patients with multiple sulphatase deficiency (1983)
    Springer
    Journal of inherited metabolic disease 6 (1983), S. 167-172 
    Details
    ISSN: 1573-2665
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Multiple sulphatase deficiency (MSD) in man is inherited as an autosomal recessive trait and associated with deficient activities of various sulphohydrolases. Cultured fibroblasts from seven different patients were assayed for arylsulphatases-A,-B and-C activities. On the basis of the results, they may be classified into three groups: I, deficient in all three arylsulphatases: II, deficient only in arylsulphatases-A and-C with half or near-normal arylsulphatase-B; electrophoretically, arylsulphatase-A activity bands are undetectable as in metachromatic leukodystrophy; III, same as in II except electrophoretically, the residual arylsulphatase-A is detectable as faint activity bands similar to those in pseudo arylsulphatase-A deficiency. In addition to the variability among different strains, within the same strain of MSD or normal cells, each enzyme activity increased several fold with increasing time in culture. These sources of biochemical variability among and within different cell strains have not been recognized before in the study of this apparently monogenic trait with multiple enzyme deficiencies. They may account for some of the discrepancies reported in the literature on arylsulphatase activities among cultured cells from different multiple sulphatase deficient patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02310875
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  • 8
    Electronic Resource
    Electronic Resource
    An ultrastructural study of sympathetic ganglion satellite cells in the rat 2. Effect of preganglionic sympathectomy (1976)
    Springer
    Journal of neural transmission 38 (1976), S. 43-57 
    Details
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The ultrastructure of satellite cells of the rat superior cervical ganglion was studied following preganglionic sympathectomy. Several distinct morphological alterations were observed: (a) enlargement of the intercellular space between the ganglion cells and the satellite cells, (b) dilation of the granular endoplasmic reticulum and loss of attached ribosomes, and (c) swelling of the mitochondria with disorganization of the cristae mitochondriales. The presence of degenerating nerve fibers and synaptic boutons was also noted.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01254139
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  • 9
    Electronic Resource
    Electronic Resource
    Somatic cell hybridization of Roberts syndrome and normal human fibroblasts transfected with plasmids carrying dominant selection markers (1987)
    Springer
    Somatic cell and molecular genetics 13 (1987), S. 245-252 
    Details
    ISSN: 1572-9931
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Roberts syndrome (RS) is a rare human recessive disorder involving, in the chromosomes of some patients, a characteristic puffing or splitting apart of the constitutive heterochromatin (the RS effect). We carried out somatic cell hybridizations between an RS cell strain (R22) with the heterochromatin abnormality and a hypoxanthine phosphoribosyltransferase-deficient cell strain (GM1662) with normal chromosome structure to determine if the presence of the normal genome would correct the RS effect in the hybrid cells. In order to provide the fibroblast strains with dominant selection markers for the hybridizations, GM1662 was transfected with the plasmid pSV3neo which conferred resistance to the antibiotic G418, and R22 was transfected with the plasmid pSV3gpt which provided resistance to mycophenolic acid. Two somatic cell hybridizations were carried out: (1) R22×GM1662 pSV3neo and (2) R22 pSVgpt×GM1662 pSV3neo. The RS effect was found to be absent in 95% and 92%, respectively, of the 200 hybrid cells examined in each experiment. This indicated that the GM1662 genome was able to correct the RS effect. The presence of the RS effect in a few of the hybrid cells was attributed to the unstable karyotype resulting from pSV3 transfection which presumably caused the loss of the normal allele(s) of the RS gene in these hybrid cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01535206
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  • 10
    Electronic Resource
    Electronic Resource
    Growth of recombinant fibroblasts in alginate microcapsules (1994)
    New York, NY [u.a.] : Wiley-Blackwell
    Biotechnology and Bioengineering 43 (1994), S. 925-933 
    Details
    ISSN: 0006-3592
    Keywords: recombinant human growth hormone ; mouse Ltk- cells ; transplantation ; gene therapy ; Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Process Engineering, Biotechnology, Nutrition Technology
    Notes: To develop a novel strategy of nonautologous somatic gene therapy, we now demonstrate the feasibility of culturing genetically modified fibroblasts within an immunoprotective environment and the optimal conditions required for their continued survival in vitro. When mouse Ltk- fibroblasts transfected with the human growth hormone gene were enclosed within permselective microcapsules fabricated from alginate-polylysine-alginate, they continued to secrete human growth hormone at the same rates as the nonencapsulated cells. They also continued to proliferate in vitro for at least 1 month even though their viability gradually declined to about 50%. The viability can be improved by controlling for (a) temperature during encapsulation, (b) duration of treatment with polylysine, (c) duration of liquefying the core alginate with sodium citrate, and (d) cell density at the time of encapsulation. The best conditions leading to improved survival and maximum proliferation of cells within the microcapsules were obtained by encapsulating the cells at 4 to 10°C instead of room temperature, coating the microspheres with polylysine for 6 to 10 min instead of 20 min, liquefying the core alginate by treating with citrate for 20 min instead of 6 to 10 min, and using a concentration of 2 × 106 cells/mL of alginate for encapsulation. Under such conditions, normally adherent and genetically engineered mouse fibroblasts survived and proliferated optimally within the microcapsule environment. The encapsulated fibroblasts maintained their level of transgene expression while recombinant gene products such as human growth hormone could diffuse through the microcapsule membrane without impediment. The demonstration that genetically modified fibroblasts can survive and continue to deliver recombinant gene products from within these microcapsules and the optimization for their maximal viability and growth within microcapsules should increase the potential for success in using such microencapsulated recombinant cells for somatic gene therapy. © 1994 John Wiley & Sons, Inc.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/bit.260431005
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