Biomedical subjects
Publications and source records attributed to J M Trujillo.
A new method of starch-gel electrophoresis using a technique of staining dependent on enzyme activity has been employed to demonstrate the isozymes of aldolase from a variety of human, rat, and frog tissues. Five of these isozymes were detected in man, seven in the rat, and at least four in the frog. The abilities of these isozymes to cleave fructose-1 ,6-diphosphate and fructose-1-phosphate were compared.
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Explore the source record for details and available documents.
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A 60-year-old woman presented with diffuse lymphadenopathy. Diagnostic and staging work-up showed that the patient had diffuse small cleaved cell lymphoma (diffuse poorly differentiated lymphocytic lymphoma) with associated histiocytes (lymphoepithelioid cell lymphoma) by the Kiel classification system. Immunohistologic staining showed a T suppressor cell tumour phenotype. Cytogenetic studies revealed the Philadelphia chromosome (Ph1). On DNA studies, the breakpoint cluster region (BCR) gene was not rearranged suggesting that the Ph1 involvement was not identical to that seen in chronic myelogenous leukemia (CML). This case is presented because of the rarity of Ph1 in lymphoid malignancies, particularly in those of T-cell origin, and because of its potentially adverse implications.
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Activation of cellular proto-oncogenes as a result of chromosomal abnormalities has been implicated in the development of some human malignancies. Perhaps one of the most striking examples of this association occurs in chronic myelogenous leukaemia, where the Philadelphia (Ph) translocation results in substitution of the 5' end of the c-abl proto-oncogene with bcr gene sequences. A unique hybrid bcr-abl message is produced. As the Ph translocation is also present in some patients with acute lymphoblastic leukaemia, we initiated studies to determine if similar genomic events occur in these two different forms of Ph-positive leukaemia. Here we report that the Ph translocation in acute lymphoblastic leukaemia can result in production of a novel aberrant c-abl protein that is distinct from the bcr-abl protein found in Ph-positive chronic myelogenous leukaemia. Our observations suggest that alternative mechanisms of activation of c-abl exist, and may be important in the development of human acute lymphoid rather than chronic myeloid malignancies.
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T and B lymphocyte populations were monitored in the peripheral blood of two long-term plateletpheresis donors. The studies showed minimal fluctuation of both populations compared to the normal controls. The evidence so far accumulated seems to indicate that long-term manual plateletpheresis has no appreciable effect on the level of the T and B cell population of the peripheral blood. Further studies are needed to evaluate larger donor pools.
A basic overview of bar code technology is presented with a focus on applications in the clinical laboratory. Bar codes operate based on symbology, a pattern of bars and white spaces that define alphanumeric characters. The codes are read by scanners, which may be stationary or handheld. Bar codes may be printed using any of several available methods. Bar codes are currently being implemented in several areas of health care, including materials management, clinical laboratory, pharmacy, medical records, and asset management. Planning for implementation of a bar code system is very much like computer installation, in terms of systems analysis and design, procedures, and training. Clinical laboratories should consider use of bar code systems, as they often are faster, better, and more cost-effective than available alternatives.
We previously reported that two multidrug resistant sublines, AdR1.2 and SRA1.2, derived from LoVo human colon carcinoma cells, apparently expressed different resistance phenotypes including differential expression of p-glycoprotein (Pgp). Here, we further examined and compared other potential resistance mechanisms between AdR1.2 and SRA1.2 resistant cells. Our results showed that the Pgp-mediated AdR1.2 cells possessed an activated drug efflux pump and decreased nucleus binding of Adriamycin, while the non-Pgp-mediated SRA1.2 cells only held the second feature. Verapamil, however, partially reversed resistance in both sublines. Although glutathione-s-transferase was overexpressed in AdR1.2 but not in SRA1.2, both sublines had lower susceptibilities to drug-induced DNA strand breaks and greater capacities to repair such damage than did LoVo cells. These data suggest that, despite the differences in multidrug resistance phenotypes, the features of decreased susceptibility to DNA damage and enhanced DNA repair capacities may represent the common mechanisms responsible for drug resistance in both Pgp- and non-Pgp-mediated multidrug resistant cells.
1-(isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7), a potent inhibitor of protein kinases, has been used as a tool to examine the role of protein kinases in a variety of cellular functions. Contingent on the cell type, H-7 has been reported either to inhibit or to promote differentiation. The biological effects of H-7 on human colon adenocarcinoma cells have not been reported. In this study we investigated the effects of H-7 on differentiation - related parameters such as cellular morphology, proliferation, the expression of carcinoembryonic antigen (CEA), fibronectin and cytokeratins in human adenocarcinoma cell lines HCT116 and SW480. H-7 induced pronounced morphological alterations in both cell lines. It induced fibronectin expression and down-modulated CEA expression and secretion in the SW480 cells, but not in the HCT116 cells. Expression of acidic keratins was not affected by H-7 treatment in both cell lines. However, the expression of basic keratins were down-modulated in the HCT116 cells and enhanced in the SW480 cells. These studies showed that the protein kinase inhibitor, H-7, modulated phenotypic properties in human colon adenocarcinoma cells. Alterations in phenotypic properties and their significance in regard to the induction of differentiation are discussed.
Six established human colon carcinoma cell lines that segregated into three groups with different degrees of differentiation were treated using three subclasses of interferons as single agents and in combination with either 5-fluorouracil, cis-platinum, or adriamycin. The cytotoxicities of the combination treatments were heterogeneous and did not relate to the cell's levels of differentiation. Our data suggest that the optimal combinations of interferons and chemotherapeutic agents are independent of the differentiation state of the colon cancer cells.
Metronidazole (MZ) was evaluated as a single agent or in combination with CDDP and araC for its cytotoxic effects on five established human colon carcinoma cell lines. MZ alone produced little cytotoxicity at 1 h drug incubation. The cytotoxicity was detectable only after 2 h incubation and increased as a function of duration of treatment, suggesting a time-dependent rather than a dose-dependent cytotoxic effect. MZ had no effect on CDDP- or araC-induced cytotoxicity, whereas MZ enhanced the synergism resulting from the combination of two antitumor agents on the human colon tumor cell lines tested. Such enhancement was more pronounced on cells growing in stationary rather than in exponential phase. MZ not only produced a reversible S-phase arrest but also lessened the CDDP-produced inhibition on the incorporation of araC into DNA. However, it did not enhance CDDP-induced DNA cross-linkings, with or without araC. Our results indicated that MZ enhanced the synergism produced by two antitumor drugs in combination and that enhancement was accompanied by an increase in S-phase population and of the incorporation of araC into nucleic acids.
We previously reported that the combination of cis-diamminedichloroplatinum (CDDP) and 1-beta-D-arabinofuranosylcytosine (ara-C) induced a remarkable synergistic killing effect on an established human colon carcinoma cell line, LoVo. The current study investigated whether this effect was LoVo specific or could be extended to other colon cancer cell lines as well as to cell lines of different histological origins, including an estrogen receptor-positive breast cancer cell line (MCF7), an ovarian cancer cell line (OV1225), and an esophageal cancer cell line (Hcu18). The six human colorectal cancer cell lines included in this study represent three biological groups with distinct phenotypic properties. Group 1 (well-differentiated) consisted of LoVo and SW48; group 2 (intermediately differentiated) comprised SW480 and SW620; and group 3 (undifferentiated) was represented by SW403 and SW1116. No significant synergistic cytotoxicity was noted after the breast and ovarian cancer cells were treated. However, synergistic lethal effects were observed in all of the six colon cancer cell lines as well as the esophageal cancer cell line. The synergistic effect on the gastrointestinal cancer cell lines was related to the concentration of ara-C and CDDP during treatment. Our results suggest that the cytotoxic synergism between ara-C and CDDP may be tissue-type specific and that synergism may depend on the histological origin of the cancer.