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Biomedical subjects

D Patterson

Publications and source records attributed to D Patterson.

At least 217 records · Page 12Linked to original sources
PubMed1983

Cholestasis due to compression of the common bile duct by pancreatic pseudocysts.

We studied 10 patients with pancreatitis who had persistent cholestasis secondary to compression of the common bile duct by a pancreatic pseudocyst. Elevation of the serum bilirubin or alkaline phosphatase levels, or both, (sensitive indicators of cholestasis) was present in each of our patients. The diagnosis of a pancreatic pseudocyst is best made by CAT scan and ultrasonography. These techniques will delineate the small intrapancreatic pseudocyst that otherwise may be difficult to recognize on inspection at operation. Endoscopic retrograde cholangiography and pancreatography are desirable because they delineate the anatomic alterations of the pancreatic and common bile ducts and may contribute information pertaining to the possibility of common duct obstruction by pancreatic fibrosis. In our opinion, cholestasis secondary to bile duct compression by a pseudocyst is an indication for operation. Each of our 10 patients had drainage of their pseudocysts. Cystoduodenostomy, performed in seven patients, was the method most commonly used. If there is concern regarding the patency of the common duct after drainage of the cyst, intraoperative cholangiography should be performed. This was carried out in three patients. In each patient, the preoperative elevations of serum alkaline phosphatase and serum bilirubin levels returned to normal limits after operative decompression of a pancreatic pseudocyst alone without an accompanying or subsequent bilioenteric bypass being required.

Cholestasis↗
PubMed1982

Effects of caffeine on pyrimidine biosynthesis and 5-phosphoribosyl 1-pyrophosphate metabolism in Chinese hamster cells.

Caffeine, at doses which enhance killing by UV light, inhibits the biosynthesis of pyrimidines in Chinese hamster ovary cells (K1) in culture. This inhibition was measured as a decrease in [14C]UTP and [14C]CTP accumulation after a 3-h incubation with [14C]aspartate or [14C]orotate and a similar decrease in Urd-A cells (which lack the first three enzymes of the pathway) using [14C]orotate as substrate. There was no such inhibition in Urd-C cells (which lack the last two enzymes) using [14C]aspartate as substrate and measuring accumulation of orotate. There is some inhibition of the fifth enzyme of the pathway, orotate phosphoribosyltransferase by caffeine in vitro and this is most striking at low 5-phosphoribosyl 1-pyrophosphate concentrations. The level of 5-phosphoribosyl 1-pyrophosphate is decreased in Chinese hamster ovary K1 cells by about 20% after 3 h and by about 70% after 16 h in the presence of caffeine. It is suggested that inhibition of pyrimidine biosynthesis by caffeine over a 16-h period may be due mainly to decreased intracellular 5-phosphoribosyl 1-pyrophosphate levels but that in the decrease in pyrimidine accumulation over 3 h, direct inhibition of orotate phosphoribosyltransferase by caffeine may also play a role.

Animals↗
PubMed1982

Giemsa-11 technique. Applications in the chromosomal characterization of hematologic specimens.

Use of the Giemsa-11 procedure for the localization of heterochromatic regions of human chromosomes and for differentiation of primate and rodent chromosomes has been somewhat limited since its discovery in 1972. An adaptation of this technique to the cytogenetic characterization of hematologic specimens has aided in the interpretation of translocations, deletions, and inversions involving human chromosome 9. The chromosomal analyses of 10% of over 100 patients, principally leukemic, were aided through the use of this auxiliary procedure. The diseases of these patients are given and portions of karyotypes are presented to show clarification of abnormalities made possible through the use of the Giemsa-11 technique.

Azure Stains↗
PubMed1982

Human c-myc onc gene is located on the region of chromosome 8 that is translocated in Burkitt lymphoma cells.

Human sequences related to the transforming gene (v-myc) of avian myelocytomatosis virus (MC29) are represented by at least one gene and several related sequences that may represent pseudogenes. By using a DNA probe that is specific for the complete gene (c-myc), different somatic cell hybrids possessing varying numbers of human chromosomes were analyzed by the Southern blotting technique. The results indicate that the human c-myc gene is located on chromosome 8. The analysis of hybrids between rodent cells and human Burkitt lymphoma cells, which carry a reciprocal translocation between chromosomes 8 and 14, allowed the mapping of the human c-myc gene on region (q24 leads to qter) of chromosome 8. This chromosomal region is translocated to either human chromosome 2, 14, or 22 in Burkitt lymphoma cells.

Burkitt Lymphoma↗
PubMed1982

Somatic cell genetic approaches to Down's syndrome.

Somatic cell genetic analysis of mutants of Chinese hamster ovary cells with deficient purine synthesis and of hybrids between these mutants and human cells is described. Data are presented substantiating that two genes for enzymes of purine synthesis, AdeC and AdeG, can be coordinately regulated in mammalian cells. Analysis of a human-hamster hybrid cell, Ade C/21, which contains a normal complement of hamster chromosomes and human chromosome 21 as its only human genetic component recognizable by electrophoretic and immunogenetic techniques demonstrates that genes associated with the presence of human chromosome 21 and required for the synthesis of specific polypeptides and specific human lethal cell surface antigens can be detected in these hybrids.

Animals↗
PubMed1982

Down's syndrome as a model disease.

Aneuploid chromosomal disorders may offer insight into the pathogenesis of certain common diseases. The birth defects and mental retardation that characterize Down's syndrome are well recognized. In addition, the altered chromosomal content that occurs in the syndrome apparently affects the prevalence of a variety of disorders, such as malignancy, endocrine dysfunction, infection, atherosclerosis, and premature aging. Because the single distinguishing factor in Down's syndrome is the presence of an excess of a part of chromosome 21, the genetic information contained in this chromosomal segment seems to be responsible for the disease manifestations. Techniques of somatic cell genetics and molecular biology allow mapping of human genes and study of their expression. With such methods it should be possible to understand Down's syndrome and other aneuploid disorders and to apply these considerations to other areas of medicine.

Adolescent↗
PubMed1981

Hydrogen peroxide causes the fatal injury to human fibroblasts exposed to oxygen radicals.

Oxygen radicals are suspected as being a cause of the cellular damage that occurs at sites of inflammation. The phagocytic cells that accumulate in areas of inflammation produce superoxide, hydrogen peroxide, hydroxyl radical, and probably singlet oxygen in the extracellular fluid. The mechanism by which these oxygen molecules kill cells is unknown. To determine which of the oxygen species is responsible for the cellular killing, we exposed human fibroblasts in culture to oxygen radicals generated by the enzymatic action of xanthine oxidase upon acetaldehyde. Using the amount of chromium-51 released from labeled fibroblasts as an index of cellular death, we found that cells were protected only by interventions that reduce hydrogen peroxide concentration. Agents that inactivate superoxide, hydroxyl radical, and singlet oxygen were ineffective in limiting oxygen radical-induced cellular death.

Cell Survival↗
PubMed1981

Two-dimensional electrophoresis of human-CHO cell hybrids containing human chromosome 11.

Two-dimensional electrophoresis-electrofocusing with polyacrylamide gels is described in which the pattern of peptide spots obtained from hybrid cells of CHO containing the single human chromosome 11 are compared with those from the hybrid which has undergone reversion so as to lose this chromosome. At least eight distinct spots unique to the cell containing chromosome 11 have been located on the electrophoretogram. Experiments are described demonstrating applicability of the method to hybrids containing specific deletion mutants of chromosome 11, an approach which makes possible regional mapping of the loci responsible for specific peptides. The methodology appears applicable to study of gene expression under the influence of hormones and other agents and to the comparison of normal and disease situations.

Animals↗
PubMed1981

Assignment of the gene coding for phosphoribosylglycineamide formyltransferase to human chromosome 14.

Purine-requiring Chinese hamster ovary cell auxotrophs of the complementation class ade-E were hybridized with various human cells, and hybrids were isolated under selective conditions in which the retention of the complementing gene on the human chromosome is necessary for survival. Synteny analysis in 72 primary and secondary hybrid clones using isozyme, karyotypic, and biochemical methods provides evidence for an assignment of the gene for phosphoribosylglycineamide formyltransferase (GART, EC 2.1.2.2), deficient in ade-E mutants, to human chromosome 14. The importance of this gene assignment to the development of hypotheses regarding the organization, structure, and regulation of genes involved in the same biosynthetic pathway in mammalian cells is discussed.

Acyltransferases↗
PubMed1981

Demonstration, by somatic cell genetics, of coordinate regulation of genes for two enzymes of purine synthesis assigned to human chromosome 21.

A method for determining coordinate genetic regulation is proposed for mammalian cells. The method involves (i) isolation of a set of mutants defective in the relevant pathway; (ii) complementation analysis of these mutants to determine dominance and to categorize the mutants into various different complementation groups; (iii) determination of the biochemical blocks in the mutants; (iv) identification of individual mutants that fail to complement the members of at least two distinct complementation groups that complement each other, such mutants being said to show coordinate regulation of the affected functions; (v) biochemical and reversion analysis of the relevant cell types to confirm the basis for the observed coordinate regulation; (vi) assignment of the individual genes to particular human chromosomes; (vii) mapping of the genes to determine contiguity on the genome; and (viii) examination of the structure of the relevant gene products. This method has allowed the demonstration of coordinate regulation between the gene coding for phosphoribosylglycineamide synthetase [5-phosphoribosylamine:glycine ligase (ADP-forming), EC 6.3.4.13], defective in our Ade-C mutants, and the gene coding for phoshoribosylaminoimidazole synthetase [5'-phosphoribosylformylglycinamidine cyclo-ligase (ADP-forming), EC 6.3.3.1], defective in our Ade-G mutants. Moreover, both genes can be assigned to human chromosome 21. Because at least two genes for purine biosynthesis have now been assigned to chromosome 21, and because patients with trisomy 21 (Down syndrome) show increased levels of serum purines, it may be that cells of these patients overproduce purines and that this overproduction may be relevant to the pathology of the syndrome.

Animals↗
PubMed1980

Isolation and characterization of 5-fluorouracil-resistant mutants of Chinese hamster ovary cells deficient in the activities of orotate phosphoribosyltransferase and orotidine 5'-monophosphate decarboxylase.

A rapid, simple method for isolation of large numbers of Chinese hamster ovary cell (CHO-K1) mutants deficient in the final two enzymes of UMP biosynthesis, orotate phosphoribosyltransferase (EC 2.4.2.10), and OMP decarboxylase (EC 4.1.1.23) is described. The method takes advantage of the fact that CHO-K1 cells require orotate phosphoribosyltransferase to activate the pyrimidine analog 5-fluorouracil to its active form; hence, mutants lacking thhe relevance of these observations to the metabolism of this cancer chemotheraputic agent, to the study of the structure of the protein(s) involved in catalyzing the last two steps of UMP biosynthesis, to the study of the structure of the gene(s) coding for this protein, and to analysis of the human genetic disease orotic aciduria is discussed.

Animals↗