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  • 1995-1999  (8)
  • 1915-1919
  • Cell & Developmental Biology  (6)
  • Complications  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Diseases of the colon & rectum 39 (1996), S. 605-609 
    ISSN: 1530-0358
    Keywords: Colostomy closure ; Hartmann's pouch ; Stoma ; Complications
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract PURPOSE: We retrospectively reviewed the records from our past five years of experience with colostomy closure at a large multispecialty hospital to determine postoperative morbidity. RESULTS: From March 1988 to April 1993, 46 patients underwent colostomy closure. Patients ranged in age from 24 to 87 (mean, 41.8) years, and 25 (54 percent) were women. Stomas had been created during emergency operations in 40 patients (87 percent); most operations (54 percent) were for complications of acute diverticulitis. Of the 46 procedures, 40 (87 percent) were end colostomies, and 6 were loop colostomies. Stomas were closed at a range of 11 to 1,357 days after creation (mean, 207 days; median, 116 days). Twenty-six patients (57 percent) underwent colostomy closure alone, and the remainder underwent additional procedures ranging from appendectomy to hepatic lobectomy. Duration of operations ranged from 1 to 9.5 (mean, 4.2) hours, and estimated blood loss averaged 400 ml. Overall hospital stay for closure was 6 to 62 (mean, 11.5) days. Inpatient complications occurred in 15 percent of patients, including congestive heart failure (2 percent), cerebrovascular accident (4 percent), pneumonia (2 percent), enterocutaneous fistula (2 percent), and pulmonary embolus with death (2 percent). The most common longterm complication was midline wound hernia, which occurred in 10 percent of surviving patients. Overall, complications occurred in 24 percent.CONCLUSIONS: Colostomy closure is a major operation; however, with good surgical judgment and technique, associated morbidity and mortality can be minimized.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1530-0358
    Keywords: Adhesions ; Complications ; Small-bowel obstruction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract PURPOSE: The study contained herein was undertaken to establish the incidence of small-bowel obstruction, adhesiolysis for obstruction, and additional abdominal surgery after open colorectal and general surgery. METHODS: A retrospective cohort study was performed using patient-specific Health Care Financing Administration data to evaluate a random 5 percent sample of all Medicare patients who underwent surgery in 1993. Of these, 18,912 patients had an index abdominal procedure. Two-year follow-up data documented outcomes of hospitalizations with obstruction, adhesiolysis for obstruction, and/or additional open colorectal or general surgery. RESULTS: Within two years of incision, excision, and anastomosis of intestine (International Classification of Diseases (ICD)-9 code 45), 14.3 percent of patients had obstructions, 2.6 percent required adhesiolysis for obstructions, and 12.9 percent underwent additional open colorectal or general surgery. After other operations of intestine (ICD code 46), 17 percent of patients had obstructions, 3.1 percent required adhesiolysis for obstructions, and 20.2 percent underwent additional open colorectal or general surgery. After operations of rectum, rectosigmoid, and perirectal tissue (ICD code 48), 15.3 percent of patients had obstructions, 5.1 percent required adhesiolysis for obstructions, and 16.4 percent underwent additional open colorectal or general surgery. After other operations on the abdominal region (ICD code 54), 12.4 percent of patients had obstructions, 2.3 percent required adhesiolysis for obstructions, and 8.8 percent underwent additional open colorectal or general surgery. CONCLUSIONS: In this retrospective study of Medicare patients, we learned that bowel obstruction, adhesiolysis for obstructions, and additional abdominal surgery occurred more often after abdominal surgery than was previously published.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 24-31 
    ISSN: 0730-2312
    Keywords: growth control ; transcription ; repression ; dihydrofolate reductase ; retinoblastoma ; Balb/c 3T3 cells ; TATAA-less promoter ; gene expression ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Dihydrofolate reductase activity is required for many biosynthetic pathways including nucleotide synthesis. Its expression is therefore central to cellular growth, and it has become a key target for cancer chemotherapy. Transcription of the dihydrofolate reductase gene is regulated with growth, being expressed maximally in late G1/early S phase following serum stimulation of quiescent cells. This regulation is directed by a promoter which contains binding sites for only the transcription factors Sp1 and E2F. In this study, the role of these promoter elements in growth/cell cycle regulation of dihydrofolate transcription was addressed directly by transient transfection of Balb/c 3T3 cells with mutant promoter-reporter gene constructs. The E2F sites were found to repress transcription in G0 and early G1 but did not contribute to the level of transcription in late G1/S phase. In contrast, Sp1 sites were able to mediate induction of transcription from the dihydrofolate reductase promoter, as well as a heterologous promoter, following serum stimulation of quiescent cells. These findings add dihydrofolate reductase to a growing list of genes at which E2F sites are primarily repressive elements and delineate a role for Sp1 sites in the growth/cell cycle regulation of transcription. J. Cell. Biochem. 67: 24-31, 1997. © 1997 Wiley-Liss, Inc.
    Additional Material: 4 Ill.
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  • 4
    ISSN: 0730-2312
    Keywords: immunocytochemistry ; breast cancer ; monoclonal antibody ; subcellular localization ; confocal microscopy ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The arsenite-stimulated human ATPase (hASNA-I) protein is a distinct human ATPase whose cDNA was cloned by sequence homology to the Escherichia coli ATPase arsA. Its subcellular localization in human malignant melanoma T289 cells was examined to gain insight into the role of hASNA-I in the physiology of human cells. Immunocytochemical staining using the specific anti-hASNA-I monoclonal antibody 5G8 showed a cytoplasmic, perinuclear, and nucleolar distribution. Subcellular fractionation indicated that the cytoplasmic hASNA-I was soluble and that the perinuclear distribution was due to association with the nuclear membrane rather than with the endoplasmic reticulum. Its presence in the nucleolus was confirmed by showing colocalization with an antibody of known nucleolar specificity. Further immunocytochemical analysis showed that the hASNA-I at the nuclear membrane was associated with invaginations into the nucleus in interphase cells. These results indicate that hASNA-I is a paralogue of the bacterial ArsA protein and suggest that it plays a role in the nucleocytoplasmic transport of a nucleolar component. J. Cell. Biochem. 71:1-10, 1998. © 1998 Wiley-Liss, Inc.
    Additional Material: 5 Ill.
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  • 5
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Molecular Reproduction and Development 42 (1995), S. 477-485 
    ISSN: 1040-452X
    Keywords: MAP kinase activation pathways ; Inter-pathway signal coordination ; MEK specificity ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology
    Notes: In the budding yeast, Saccharomyces cerevisiae, four separate but structurally related mitogen-activated protein kinase (MAPK) activation pathways are known. The best understood of these regulates mating. Pheromone binding to receptor informs cells of the proximity of a mating partner and induces differentiation to a mating competent state. The MARK activation cascade mediating this signal is made up of Ste 11 (a MEK kinase [MEKK]), Ste7 (a MAPK/ERK kinase [MEK]), and the redundant MAPK-related Fus3 and Kss1 enzymes. Another MAPK activation pathway is important for cell integrity and regulates cell wall construction. This cascade consists of Bck1 (a MEKK), the redundant Mkk1 and Mkk2 enzymes (MEKs), and Mpk1 (a MAPK). We exploited these two pathways to learn about the coordination and signal transmission fidelity of MAPK activation cascades.Two lines of evidence suggest that the activities of the mating and cell integrity pathways are coordinated during mating differentiation. First, cells deficient in Mpk1 are susceptible to lysis when they make a mating projection in response to pheromone. Second, Mpk1 activation during pheromone induction coincides with projection formation. The mechanism underlying this coordination is still unknown to us. Our working model is that projection formation generates a mobile second messenger for activation of the cell integrity pathway.Analysis of a STE7 mutation gave us some unanticipated but important insights into parameters important for fidelity of signal transmission. The Ste7 variant has a serine to proline substitution at position 368. Ste7-P368 has higher basal activity than the wild-type enzyme but still requires Ste 11 for its function. Additionally, the proline substitution enables the variant to transmit the signal from mammalian Raf expressed in yeast. This novel activity suggests that Ste7-P368 is inherently more permissive than Ste7 in its interactions with MEKKs. Yet, Ste7-P368 cross function in the cell integrity pathway occurs only when it is highly overproduced or when Ste5 is missing. This behavior suggests that Ste5, which has been proposed to be a tether for the kinases in the mating pathway, contributes to Ste7 specificity and fidelity of signal transmission. © 1995 wiley-Liss, Inc.
    Additional Material: 7 Ill.
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  • 6
    ISSN: 1058-8388
    Keywords: Collagen ; Fibril growth ; Fibrillogenesis ; Tendon ; Decorin ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Elucidating how collagen fibril growth is regulated is important in determining how tissues are assembled. Fibrils are deposited as segments. The growth of these segments is an important determinant of tissue architecture, stability, and mechanical attributes. Fibril segments were isolated from developing tendons and their structure characterized. The post-depositional changes leading to linear and lateral growth of fibrils also were examined. Segments extracted from 14-day chicken embryo tendons had a mean length of 29 μm. The segments were asymmetric, having a short and a long tapered end. Most of the segments were centrosymmetric with respect to molecular packing. Segments extracted from 12-to 16-day tendons had the same structure, but mean segment length increased incrementally due to the addition of an increasingly large population of longer segments. At 17 days of development there was a precipitous increase in segment length. The morphological data indicate that the increase in length was the result of lateral associations among adjacent segments. Analysis demonstrated that this fibril growth was associated with a significant decrease in fibril associated decorin. Using immunoelectron microscopy, decorin was seen to decrease significantly at 18 days of development. When decorin content was biochemically determined, a decrease also was observed. Decorin mRNA also decreased relative to fibrillar collagen mRNA during the same period. These data support the hypothesis that a decrease in fibril-associated decorin is necessary for fibril growth associated with tissue maturation. Growth through post-depositional fusion allows for appositional and intercalary growth and would be essential for normal development, growth, and repair. © 1995 Wiley-Liss, Inc.
    Additional Material: 11 Ill.
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  • 7
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Retinoids are currently being tested for the treatment and prevention of several human cancers, including breast cancer. However, the anti-cancer and growth inhibitory mechanisms of retinoids are not well understood. All-trans retinoic acid (RA) inhibits the growth of the estrogen receptor-positive (ER+) breast cancer cell line, MCF-7, in a reversible and dose-dependent manner. In contrast, insulin-like growth factors (IGF-I,IGF-II) and insulin are potent stimulators of the proliferation of MCF-7 and several other breast cancer cell lines. Pharmacologic doses of RA (≤10-6M) completely inhibit IGF-I-stimulated MCF-7 cell growth. Published data suggest that the growth inhibitory action of RA on IGF-stimulated cell growth is linear and dose-dependent, similar to RA inhibition of unstimulated or estradiol-stimulated MCF-7 cell growth. Surprisingly, we have found that IGF-I or insulin-stimulated cell growth is increased to a maximum of 132% and 127%, respectively, by cotreatment with 10-7 M RA, and that 10-9-10-7 M RA increase cell proliferation compared to IGF-I or insulin alone. MCF-7 cells that stably overexpress IGF-II are also resistant to the growth inhibitory effects of 10-9-10-7 M RA. Treatment with the IGF-I receptor blocking antibody, αIR-3, restores RA-induced growth inhibition of IGF-I-treated or IGF-II-overexpressing MCF-7 cells, indicating that the IGF-I receptor is mediating these effects. IGFs cannot reverse all RA effects since the altered cell culture morphology of RA-treated cells is similar in growth-inhibited cultures and in IGF-II expressing clones that are resistant to RA-induced growth inhibition. These results indicate that RA action on MCF-7 cells is biphasic in the presence of IGF-I or insulin with 10-9-10-7 M RA enhancing cell proliferation and ≥ 10-6M RA causing growth inhibition. As IGF-I and IGF-II ligands are frequently detectable in breast tumor tissues, their potential for modulation of RA effects should be considered when evaluating retinoids for use in in vivo experimental studies and for clinical purposes. Additionally, the therapeutic use of inhibitors of IGF action in combination with RA is suggested by these studies. © 1995 Wiley-Liss Inc.
    Additional Material: 7 Ill.
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  • 8
    Electronic Resource
    Electronic Resource
    New York, NY : Wiley-Blackwell
    BioEssays 19 (1997), S. 787-792 
    ISSN: 0265-9247
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: In eukaryotic cells the nucleus and its contents are separated from the cytoplasm by the nuclear envelope. Macromolecules, as well as smaller molecules and ions, can cross the nuclear envelope through the nuclear pore complex. Molecules greater than approx. 60 kDa and containing a nuclear localization signal are actively transported across the nuclear membranes, but there has been little evidence for regulatory mechanisms for smaller molecules and ions. Recently, diffusion across the nuclear envelope has been observed to be regulated by nuclear cisternal Ca2+ concentrations. Following depletion of Ca2+ from the nuclear store by inositol 1,4,5-trisphosphate or Ca2+ chelators, a fluorescent 10 kDa marker molecule was no longer able to enter the nucleus. Distinct conformational states of the nuclear pore complexes depended on the Ca2+ filling state of the nuclear envelope, supporting the assumption that a switch in the conformation of the nuclear pore complex may control the transport of intermediate-sized molecules across the nuclear envelope. Thus nuclear Ca2+ stores may regulate the conformational state of the nuclear pore complex, and thereby passive diffusion of molecules between the cytosol and the nucleoplasm. The physiological significance of this finding is currently unknown.
    Additional Material: 4 Ill.
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