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Biomedical subjects

S A Bader

Publications and source records attributed to S A Bader.

At least 19 recordsLinked to original sources
PubMed1998

"Patient informatics": creating new partnerships in medical decision making.

The amassing of health information on the Internet and World Wide Web continues unabated. Patients anxious to participate in decisions about their own treatment have turned to the Internet to confirm diagnoses, validate physician-recommended treatment, or seek alternative therapies. While increased information for patients has been linked to improved outcomes, there are inherent dangers associated with the kind of unauthenticated information available on the Web. The authors discuss the nature of these dangers as well as review the advantages for patients of "information therapy" (improved access to health information). They also examine how the Internet has begun to affect the physician-patient relationship, and describe how the Internet and information technology can be effectively used by physicians in patient care. They recommend that the academic health sciences community seize the opportunity to take the lead in ensuring that patients have access to reliable health information, and suggest that "patient informatics" be integrated by academic physicians and educators into the teaching of clinical skills.

Academic Medical Centers↗
PubMed1998

Analysis of CD44 interactions with hyaluronan in murine L cell fibroblasts deficient in glycosaminoglycan synthesis: a role for chondroitin sulfate.

CD44 is a widely expressed cell adhesion molecule that binds the extracellular matrix component, hyaluronan, in a tightly regulated manner. Previous studies have shown that the CD44-hyaluronan interaction is affected by changes in the glycosylation state of CD44. In this study, we take advantage of several well-characterized murine L cell mutants defective in heparan sulfate synthesis (gro2C cells), heparan sulfate and chondroitin sulfate synthesis (sog9 cells), and glycosaminoglycan and oligosaccharide processing (sog8 cells) to assess the effects of these defects on the hyaluronan binding ability of CD44. In parental L cells and gro2C cells, CD44 was induced to bind hyaluronan after addition of the activating, anti-CD44 monoclonal antibody, IRAWB 14. By contrast, no inducible binding was observed in sog9 cells. Treatment of L cells with sodium chlorate, an inhibitor of sulfation, also abolished inducible hyaluronan binding. However, inducible and some constitutive hyaluronan binding was observed in sog8 cells. This indicates that sulfation and, in particular, the addition of chondroitin sulfate are required for inducible hyaluronan binding by CD44 in L cells. However, in the absence of fully processed oligosaccharides, chondroitin sulfate is not essential for hyaluronan binding, indicating that the effect of chondroitin sulfate is dependent upon the glycosylation state of the cell. Thus, in addition to glycosylation, chondroitin sulfate biosynthesis is an important post-translational modification that can affect the hyaluronan binding ability of CD44.

3T3 Cells↗
PubMed1997

FHIT and FRA3B 3p14.2 allele loss are common in lung cancer and preneoplastic bronchial lesions and are associated with cancer-related FHIT cDNA splicing aberrations.

We evaluated primary lung cancers, tumor cell lines, and preneoplastic bronchial lesions for molecular genetic abnormalities in the candidate tumor suppressor gene FHIT, which spans the FRA3B fragile site at 3p14.2. 3p14.2 allele loss was very frequent in 32 lung cancer cell lines [100% of small cell lung cancer and 88% of non-small cell lung cancer (NSCLC)] and 108 primary NSCLC cancers (45%), with numerous breakpoints indicating involvement of several distinct regions in the FRA3B site. 3p14 allele loss was least frequent in the adenocarcinoma subtype and occurred at the relatively late carcinoma in situ stage of preneoplastic bronchial lesions found in NSCLC patients. Homozygous deletions within the FHIT/FRA3B region were found in 6 of 135 (4.4%) thoracic cancer cell lines. Northern blot showed low or absent FHIT expression in most thoracic cancer cell lines tested, whereas reverse transcription-PCR showed that 59-62% exhibited aberrant FHIT transcripts but nearly always (93-100%) also expressing the wild-type transcripts. Aberrant transcripts included precise deletions of FHIT exons, insertion of non-FHIT sequences between exons and insertions replacing exons. Complete open reading frame single-strand conformational polymorphism analysis of 102 lung cancer cDNAs revealed only one nonsplicing mutation. Normal cells including bronchial epithelium, lung, and trachea expressed wild-type FHIT transcript and a variant transcript deleted for exon 8 but not the other aberrant transcripts, arguing against exon 8-deleted FHIT transcripts being tumor specific. Our findings support the conclusion that FHIT/FRA3B abnormalities are associated with lung cancer pathogenesis but that FHIT abnormalities differ from the types of mutations and lack of wild-type transcript found in classic tumor suppressor genes, and functional studies are needed to define the role of FHIT in thoracic tumorigenesis.

Acid Anhydride Hydrolases↗
PubMed1997

Precise localization of the FHIT gene to the common fragile site at 3p14.2 (FRA3B) and characterization of homozygous deletions within FRA3B that affect FHIT transcription in tumor cell lines.

Chromosomal or allelic losses at 3p14 are common in a variety of human tumors, including those of the lung, breast, kidney, and head and neck. This suggests the existence of a tumor suppressor gene in this band. A promising candidate is the recently cloned FHIT gene, which spans the common fragile site, FRA3B, at 3p14.2. We previously identified a region of fragility at 3p14.2 (FRA3B) of > 85 kb by cloning DNA flanking pSV2neo integrations and constructed a partial genomic contig of the region. Using probes from the contig, we tested for deletions within this region in DNA from 105 human tumor cell lines, predominantly derived from lung cancers. We identified one gastric and four lung cancer cell lines with homozygous interstitial deletions involving the FRA3B region. The deletion in one lung cancer cell line lies entirely within our contig and is < 65 kb. We have identified, cloned, and sequenced this breakpoint junction. We have also shown that our probes lie within intron S of the FHIT gene and, furthermore, that exon 5 is located approximately 1 kb from one of our probes and, thus, lies within the region of fragility. Two lines with entirely intronic deletions yield FHIT transcripts of normal size. In one of these, this was the sole transcript identified. In the other line, an FHIT transcript completely normal in sequence was accompanied by two larger abnormal transcripts. These results leave open the possibility that some homozygous deletions within the FHIT gene are without phenotypic effect and result from genetic instability of this region. However, taken together, our results provide evidence that breakage and rearrangement within the FRA3B fragile site sequences result in alterations of FHIT and are likely to be involved in carcinogenesis.

Acid Anhydride Hydrolases↗
PubMed1995

From strategic planning to TQM: a complete management approach.

Organizations can no longer rely on a single management solution as they respond to a complex world. Biomedical communications managers need to employ a variety of management tools as they cope with a rapidly changing landscape and an increasing set of business pressures. This article describes two management strategies, strategic planning and total quality management, which can be used to achieve success in the 21st century.

Audiovisual Aids↗
PubMed1994

Molecular analysis of the HuD gene encoding a paraneoplastic encephalomyelitis antigen in human lung cancer cell lines.

Small cell lung cancer (SCLC) is known to express the HuD protein, the neuronal antigen homologous to Drosophila Elav and Sxl genes involved in neuronal and sex development. HuD is the target of an immune response including high titered antibodies causing paraneoplastic encephalomyelitis and sensory neuropathy. Because the p53 recessive oncogene is mutated and anti-p53 antibodies frequently occur in cancer patients, we wondered if the development of anti-HuD antibodies signaled the presence of HuD mutations in lung cancer. The HuD gene was mapped to chromosome region 1p using a human-mouse hybrid cell panel. We confirmed that 26 of 46 cancer (43 lung cancer and 3 mesothelioma) cell lines expressed HuD mRNA and that this expression, as well as protein expression by Western blot, correlated strongly with the SCLC neuroendocrine phenotype. Southern blot and single-strand conformation polymorphism analyses showed that HuD was not mutated in 78 lung cancers, including patients with the severe paraneoplastic syndrome. Northern blot analysis showed that lung cancer cell lines expressed two major mRNAs (4.3 and 4.0 kilobases) of HuD. We found the three previously described alternative spliced mRNA forms (HuDpro, HuD, and HuDmex). In addition, we also found HuD mRNA had an alternative splicing form in its 5'-coding region. This alternative splice introduced 87 base pairs of sequence and a termination codon resulting in a predicted small, truncated protein (11 amino acids) reminiscent of the male-specific truncated protein in the Sex-lethal (Sxl) gene of Drosophila. However, mRNAs encoding both full-length and truncated proteins were expressed in all SCLCs. These results show that the HuD gene is not mutated in lung cancer, including tumors from patients producing anti-HuD antibodies, but HuD expression is an independent marker or determinant of the neuroendocrine differentiation seen in SCLC.

Antigens, Neoplasm↗
PubMed1994

Seize the day.

Explore the source record for details and available documents.

Computer-Assisted Instruction↗
PubMed1993

Are computer-based educational materials recognized as publications? An analysis of promotion documents at American medical colleges.

A generalized perception exists that faculty will not be properly rewarded for efforts in developing computer-based educational materials. Faculty governed by traditional promotion and tenure systems thus may be reluctant to devote energies towards development of these materials. Recent national panels on educational reform have called for a reexamination of academic reward structures to insure that faculty receive appropriate scholarly recognition for materials developed in these new formats. A study of policy documents from accredited medical colleges in the United States was conducted to determine the extent to which academic health science institutions have adopted policies to grant recognition of computer-based materials equivalent to that accorded traditional print publications. Results revealed that while some progress has been made by leading-edge institutions, in three-quarters of the institutions, development of computer-based educational materials is considered evidence in support of teaching, not the more highly rewarded research or scholarly activity.

Computer-Assisted Instruction↗
PubMed1991

Dissociation of suppression of tumorigenicity and differentiation in vitro effected by transfer of single human chromosomes into human neuroblastoma cells.

The development of human neuroblastoma is associated with abnormalities of the short arm of chromosome 1 (1p). To determine the importance of sequences on that part of chromosome 1, we transferred translocated chromosomes containing normal portions of chromosome 1p or 1q into the neuroblastoma cell line NGP.1A.TR1 and also normal intact chromosomes 11 and 17 as putative controls. Transfer of chromosome t(X;1q) had no effect on any property we studied of the neuroblastoma cells. It was found that the transfer of chromosome t(X;1p) induced neuronal differentiation, but most of those cells died. The cell lines that grew out from the survivors lacked the t(X;1p) chromosome and were still tumorigenic. Transfer of chromosome 11 induced differentiation but did not affect cell proliferation or the tumorigenic phenotype. We have also demonstrated the existence of a new tumor suppressor gene on chromosome 17 that does not induce differentiation in vitro but completely suppresses the tumor-forming ability of the neuroblastoma cells. Differentiation of neuroblastoma cells in vitro and suppression of tumorigenicity are therefore controlled by multiple genes on different chromosomes and are not necessarily correlated.

Animals↗
PubMed1990

Purification and characterization of a maturation-activated myelin basic protein kinase from sea star oocytes.

A meiosis-activated myelin basic protein (MBP) kinase was purified approximately 8700-fold from soluble post-germinal vesicle breakdown extracts from maturing oocytes of the sea star Pisaster ochraceus. Purification to apparent homogeneity was achieved by sequential chromatography on DEAE-cellulose, hydroxylapatite, phosphocellulose, phenyl-Sepharose, heparin-Sepharose, polylysine-Sepharose, and Mono-Q. The final product exhibited an apparent molecular mass of approximately 42 kDa by both native gradient and sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and this precisely correlated with the chromatographic behavior of the recovered MBP kinase activity on a Superose 6/12 column. The kinase utilized the MBP as the major substrate with little or no phosphorylation of histones (H1, H2A, or H2B), casein, phosvitin, protamine, or 40 S ribosomal proteins. The purified enzyme was relatively insensitive to high concentrations of beta-glycerol phosphate, calmodulin, EGTA, NaCl, sodium fluoride, dithiothreitol, spermine, and heparin but was quite sensitive to inhibition by metal ions such as Mn2+, Zn2+, and Ca2+. The true Km values for ATP and myelin basic protein were determined to be 58 and 25 microM, respectively, using double-reciprocal plots. The purified enzyme was unable to utilize GTP in place of ATP. The enzyme was shown to rapidly undergo autophosphorylation. The autophosphorylation was sensitive to alkali treatment implying that phosphate was incorporated on serine/threonine residues. The properties of this MBP kinase are reminiscent of a protein kinase that is also activated in a cyclic fashion at M-phase during the early cell divisions of sea star and sea urchin embryos (Pelech, S. L., Tombe, R., Meijer, L., and Krebs, E. G. (1988) Dev. Biol. 130, 26-36).

Adenosine Triphosphate↗
PubMed1988

Teaching medical professionals to retrieve and manage medical information.

Popularity of the personal computer has prompted physician interest in direct access to the medical literature from sophisticated electronic data retrieval systems. This paper describes the educational programs developed by the library at the George Washington University Medical Center in response to this interest and growing national trend. As a result of these programs, the role of the librarian has changed permanently. Librarians are now perceived by faculty as educational specialists and information consultants. The evolution in libraries parallels the technological changes taking place in other biomedical communications units. The authors recommend the positive outcomes from adapting traditional roles to meet user's needs in a changing environment.

Humans↗
PubMed1987

Regulation of epitectin production in a malignant cell line.

RT112 cells, a line derived from a human bladder carcinoma, produce epitectin at very low levels in standard culture media; but production and secretion of this mucin are greatly increased when the cells are exposed to hyperosmotic conditions. It appears that hyperosmolarity, by inducing an increase in intracellular sodium, entrains an increase in intracellular free calcium. Evidence is presented for the view that it is the increase in intracellular free calcium that provides the more direct stimulus for the enhanced production of epitectin.

Amiloride↗