[Surgery of breast cancer].
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Biomedical subjects
Publications and source records attributed to R Schroeder.
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Using gel filtration, ligand-affinity chromatography and reversed phase HPLC, four insulin-like growth factor-binding proteins (IGF-BPs) have been purified from adult rat serum. Sodium dodecyl sulfate polyacrylamide gel electrophoretic (SDS-PAGE) analysis revealed that all four proteins migrated as doublets at 45/37 (peak 1 in Fig.4), 36/32 (peaks 2 and 5 in Fig. 4), 35/33 (peak 3 in Fig. 4) and 22/28 kDa (peaks 4a, 4b in Fig. 4), respectively under reducing conditions. N-terminal sequence analysis of the 45/37 kDa doublet showed that it is identical to the N-terminal of the 45 kDa rat IGF-BP whereas the 22/28 kDa doublet is the C-terminal truncated form of the 45 kDa species. The 35/33 kDa doublet has the same N-terminal sequence as that of the rat IGF-BP isolated from a BRL-3A cell line. However, the N-terminal sequence of the 36/32 kDa doublet is unique, although it may be related to the BRL-3A protein. The most abundant IGF-BP in adult rat serum corresponds to the 45 kDa species plus its C-terminal truncated forms, whereas the second most abundant IGF-BP is the novel protein detected in this study, while the least abundant species is the BRL-3A IGF-BP.
Seventeen non-directed td- (thymidylate synthase-deficient) splicing-defective mutations isolated in phage T4 were localized within the catalytic core of the ribozyme. All of the mutations occur in conserved structural elements that form part of the td intron core secondary structure. Remarkably, seven of the seventeen independently isolated mutations clustered in the dinucleotide 5' element (P6[5']) of the putative two-base-pair P6 stem. An analysis of this region was undertaken by site-directed mutagenesis of the plasmid-borne td gene, leading to the following findings: First, the short P6 pairing in the td secondary structure model was verified with appropriate P6[5'] and P6[3'] compensatory mutations. Second, all P6[5'] and P6[3'] mutants are defective in the first step of splicing, guanosine-dependent 5' splice site cleavage, whereas their activity at the 3' splice site is variable. Third, residual in vitro splicing activity of the mutants altered on only one side of the P6 pairing is correlated with the ability to form an alternative two-base-pair P6 stem. Fourth, the degree to which the compensatory mutants have their splicing activity restored is highly condition-dependent. Restoration of phenotype of the compensatory P6[5']:[3'] constructs is weak under stringent in vitro conditions as well as in vivo. This sequence specificity is consistent with phylogenetic conservation of the P6 pairing elements in group I introns, and suggests either structural constraints on the P6 stem or a dual function of one or both pairing elements.
A case of papillary-cystic (solid cystic) tumor of the pancreas in a 15-year-old woman is presented. This type of tumor is of low grade malignancy and is without endocrinological activity. It is usually found in young women. The treatment is surgical resection.
The amyloid beta protein peptide is a major constituent of amyloid plaque cores in Alzheimer's disease and is apparently derived from a higher molecular weight precursor. It is now shown that the core protein of a heparan sulfate proteoglycan secreted from a nerve cell line (PC12) has an amino acid sequence and a size very similar to those of the amyloid beta protein precursor and that these molecules are antigenically related. This amyloid beta protein precursor-related protein is not found in the conditioned medium of a variant cell line (F3 PC12) that does not secrete heparan sulfate proteoglycan. The synaptic localization and metabolism of this class of proteoglycans are consistent with its potential involvement in central nervous system dysfunction.
Corticosterone plays an important role in the regulation of postnatal development in the rat. Basal concentrations of plasma corticosterone increase markedly during the 3rd wk of life. To date, however, the physiologic bases of this increase have remained unclear. To understand the determinants of circulating concentrations of corticosterone during this period, the plasma half-life of disappearance at steady state (t1/2), the apparent volume of distribution, and metabolic clearance rate were determined after injection of a tracer dose of 3H-corticosterone in rats at 12, 16, and 22 days of age. The t1/2 for total plasma corticosterone decreased with increasing age. The volume of distribution decreased even more steeply and, consequently, the MCR displayed a highly significant decline between 12 and 22 days of age. As plasma concentrations of corticosteroid-binding globulin are known to increase markedly during this period, the t1/2 of protein-bound corticosterone was measured and that of free corticosterone was computed. At all ages the t1/2 of bound corticosterone was less than that of free corticosterone. Protein binding of the injected 3H-corticosterone increased significantly with development. Thus, increased binding of corticosterone is associated with decreased t1/2. The increasing association of corticosterone with corticosteroid-binding globulin during this developmental period is the most likely explanation for the steep decline of volume of distribution and thus of the metabolic clearance rate for corticosterone. The latter provides, for the first time, an understanding of the basis of the developmental increase in plasma concentrations of corticosterone.
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Leber's congenital amaurosis is a hereditary clinical disorder that may be associated with several different diseases. This study consists of a retrospective review of 43 cases. Twenty of our patients had fundus appearances that resembled retinitis pigmentosa. Five had normal-appearing fundi. The remainder had other, previously reported fundus abnormalities, with the exception of two patients who demonstrated a new fundus finding, a nummular pigmentary pattern. Other associated eye anomalies included cataracts, keratoconus, ptosis, and strabismus. The most frequent systemic associations were mental retardation, cystic renal disease, skeletal disorders, and hydrocephalus.
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The group of laypersons who founded St. Francis Hospital, Memphis, TN, in 1971 were dedicated to upholding Catholic values in health care yet often were questioned about the origins of their "Catholic" identity. "How can a hospital that is not owned by the diocese or sponsored by a religious institute call itself Catholic?" they were asked. The answer, St. Francis found, lies in the revised Code of Canon Law, which provides for a group of laypersons such as theirs to form a private association of the Christian faithful, be officially recognized by the Church, and receive canonical status. A participant in the pilot project through which CHA is studying the feasibility of alternative forms of sponsorship, St. Francis has worked closely with CHA in developing the private association's statutes and coordinating with the bishop provisions for evaluation of its stewardship. According to the statutes, the private association will monitor the hospital's adherence to Church values, and the bishop, serving in a pastoral capacity, will with CHA's assistance assess the association's effectiveness in carrying out its mission.
In the mitochondrial DNA of Saccharomyces cerevisiae, the genes cob-box and oxi3, coding for apocytochrome b and cytochrome oxidase subunit I respectively, are split. Several mutations located in the introns of the cob-box gene prevent the synthesis of cytochrome b and cytochrome oxidase subunit I (this is known as the 'box effect').-We have elucidated the molecular basis of this phenomenon: these mutants are unable to excise the fourth intron of oxi3 from the cytochrome oxidase subunit I pre-mRNA; the absence of a functional bI4 mRNA maturase, a trans-acting factor encoded by the fourth intron of the cob-box gene explains this phenomenon. This maturase was already known to control the excision of the bI4 intron; consequently we have demonstrated that it is necessary for the processing of two introns located in two different genes. Mutations altering this maturase can be corrected, but only partially, by extragenic suppressors located in the mitochondrial (mim2) or in the nuclear (NAM2) genome. The gene product of these two suppressors should, therefore, control (directly or indirectly) the excision of the two introns as the bI4 mRNA maturase normally does.
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During sporulation of Saccharomyces cerevisiae the mitochondria undergo a differentiation process, leading to a "spore mitochondrion", which differs both physiologically and morphologically from vegetative cell mitochondria. We report here the behaviour of the mitochondrial transcripts during this differentiation process. The circular transcripts representing spliced introns of the two mitochondrial split genes for cytochrome b and for the subunit 1 of the cytochrome c oxidase, which are very abundant during vegetative growth, are not detectable in sporulating cells. This loss does neither take place in haploid cells under sporulation conditions nor when erythromycin is added to the medium. The process of some mRNAs is advanced in relation to their precursors in sporulating cells.
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We investigated the sporulation properties of a series of diploid Saccharomyces cerevisiae strains homozygous for inositol auxotrophic markers. The strains required different amounts of inositol for the completion of sporulation. Shift experiments revealed two phases of inositol requirement during sporulation which coincided with the two phases of lipid synthesis found by earlier workers. Phase I was at the beginning and during premeiotic deoxyribonucleic acid synthesis; phase II immediately preceded the appearance of mature asci. Of the inositol taken up by sporulating cells, 90% was incorporated into inositol phospholipids. By two-dimensional thin-layer chromatography, eight compounds were resolved, one of which was sporulation specific. The majority of the inositol phospholipids were, however, identical to those found in vegetatively growing cells. In the absence of inositol, the cells did not sporulate but, after a certain time, were unable to return to vegetative growth. These nonsporulating cells did, however, incorporate acetate into lipids and double their deoxyribonucleic acid content in the premeiotic phase. We believe that it is this lack of coordination of biosynthetic events which causes inositol-less death on sporulation media without inositol.
The movement of the aortic root under resting conditions was analyzed echographically in 82 patients (32 were postoperative examinations of Björk-Shiley aortic and/or mitral valve prostheses). Additionally, ECG, PCG, carotid pulse curve or apexcardiogram were recorded simultaneously in the majority of the cases. In view of the time correlation between these noninvasive parameters, the results clearly show that both ventrally and dorsally directed motions of the aortic root during the cardiac cycle only reflect the change in volume of the left atrium. Thus aortic root motion might, if at all, be an indirect index of left ventricular stroke volume and only so if sinus rhythm is present and no mitral insufficiency or atrial septum defect exist.
Different doses of progesterone, D-norgestrel and delta 15-D-norgestrel were injected subcutaneously for 7 days to female rats castrated 7 days prior to the experiments. One day after the last steroid injection a i.p. LH-RH test was performed, blood samples were collected by heart puncture and serum levels of r-LH and r-FSH were estimated by radioimmunoassay. LH-RH serum levels were determined in progestagen treated control groups by an anterior pituitary cell culture bioassay. Dose dependent inhibitory effects of steroids on LH-RH stimulated gonadotropin release were observed and a dissociation of r-LH and r-FSH serum levels was found. The modulatory influence of progestagens used in this study on LH-RH provoked gonadotropin release correlated with their biological efficiency evaluated in the Clauberg test. Progesterone, D-norgestrel and delta 15-D-norgestrel treatment had no significant effects on basal r-LH levels, but LH-RH provoked r-LH levels were higher than in the control animals. Progesterone and D-norgestrel suppressed basal as LH-RH stimulated r-FSH levels, whereas delta 15-D-norgestrel showed a complex influence on r-FSH secretion. A progestagen stimulated rise of LH-RH serum levels was found and indicated an additional effect of these hormones at the hypothalamic level. These data suggest the action of progestagens at various levels of the hypothalamus-pituitary axis.
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