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Biomedical subjects

C W Anderson

Publications and source records attributed to C W Anderson.

176 records · Page 10Linked to original sources
PubMed1973

Processing of adenovirus 2-induced proteins.

Analysis of (35)S-methionine-labeled extracts of adenovirus 2-infected KB cells revealed 22 virus-induced polypeptide components. Most proteins of the virion were easily detected in extracts of whole cells labeled for short periods between 15 and 30 h after infection; however, several virion components were conspicuously absent. Radioactivity appeared in two of these virion components during a chase in nonradioactive medium, and this appearance was paralleled by a decrease in the radioactivity associated with two nonvirion adenovirus-induced proteins, results which imply precursor-product relationships for these components. Comparison of one of the chasable adenovirus-induced components (designated P-VII; mass of 20,000 daltons) and the major core protein (VII; mass of 18,500 daltons) of the virion showed that they have four common methionine-containing tryptic peptides; P-VII has an additional methionine residue which is not found in the major core protein. We propose that at least two of the adenovirus 2 virion components are derived by the cleavage of higher molecular weight precursor polypeptides.

Adenoviridae↗
PubMed1972

Pattern of protein synthesis in monkey cells infected by simian virus 40.

After infection of several permanent monkey cell lines by simian virus 40 (SV40), four additional protein bands can be detected by simple sodium dodecyl sulfate-polyacrylamide gel electrophoresis of whole-cell extracts. These bands appear only after the onset of viral deoxyribonucleic acid (DNA) synthesis, and inhibitors of DNA synthesis prevent their appearance. Three of them correspond to three previously identified capsid components, VP1, VP2, and VP3. The fourth protein band, which does not correspond to a previously identified virion component, is induced by SV40 infection of CV-1 and BSC-1 cultures but not by infection of MA-134 cultures.

Amino Acid Sequence↗
PubMed1971

Breakdown and exclusion of superinfecting T-even bacteriophage in Escherichia coli.

In bacterial strains containing the deoxyribonuclease endonuclease I (endonuclease I(+) strains), 70 to 80% of the injected superinfecting T-even phage deoxyribonucleic acid (DNA) is rapidly degraded to oligonucleotides having an average chain length of 8, the same value as that obtained by endonuclease I digestion of purified T-even phage DNA in vitro. In endonuclease I(-) strains, less than 5% of the injected superinfecting T-even phage DNA is degraded to acid-soluble components. The superinfecting phage DNA is, however, fragmented into a large segment having a molecular weight of about 90 x 10(6) and 30 or more small acid-insoluble segments having molecular weights of less than 10(6). In both endonuclease I(+) and endonuclease I(-) strains, over 80% of the DNA from adsorbed primary T2 or T4 phage, but only 50% of the DNA from adsorbed superinfecting T2 or T4 phage, is injected. Superinfecting T4 are genetically excluded as efficiently from endonuclease I(-) strains as they are from endonuclease I(+) strains. The excluded phage cannot complement defects in either early or late gene functions carried by the primary phage. The induction of both superinfection breakdown and superinfection exclusion requires a period of protein synthesis between primary infection and addition of the superinfecting phage. These observations seem best explained by failure of superinfecting DNA to enter the host cell cytoplasm, presumably as a result of changes in the cell envelope induced by the primary phage.

Centrifugation, Density Gradient↗
PubMed1971

Localization of parental deoxyribonucleic acid from superinfecting T4 bacteriophage in Escherichia coli.

High-resolution autoradiography has been employed to localize the nonsolubilized but genetically excluded deoxyribonucleic acid (DNA) of T4 bacteriophage superinfecting endonuclease I-deficient Escherichia coli. This DNA was found to be associated with the cell envelope (this term is used here to include all cellular components peripheral to and including the cytoplasmic membrane); in contrast, T4 DNA in primary infected cells, like host DNA in uninfected E. coli, was found to be near the cell center. The envelope-associated DNA from super-infecting phage was not located on the outermost surface of the cell since it was insensitive to deoxyribonuclease added to the medium. These results suggest that DNA from superinfecting T-even phage is trapped within the cell envelope.

Autoradiography↗
PubMedDate not supplied

Pyrrole oxidation and protein cross-linking as necessary steps in the development of gamma-diketone neuropathy.

It has been well documented that the gamma-diketone HD1 is the ultimate toxic metabolite of n-hexane. Furthermore, it has been shown that the pathogenetic mechanism by which HD exerts its neurotoxic effects is through binding to protein lysly residues and cyclization to pyrroles. The present study sought to determine whether the presence of pyrrole residues on NF1 proteins is sufficient to cause the NF-filled axonal swellings associated with n-hexane and other gamma-diketone neuropathies or whether pyrrole oxidation and protein cross-linking also have to occur in order for neurotoxicity to develop. We synthesized the HD analogue AcHD1 and assessed its rate of pyrrole formation in vitro, the ease of oxidation of its resulting pyrroles, and its ability to cross-link proteins in vitro. The in vivo effects of AcHD on rats were examined following daily ip1 injections. AcHD was found to have a rate of pyrrole formation comparable to that of the potent HD analogue DMHD1 at 35 degrees C. The pyrrole derived from AcHD was more resistant to oxidation than that derived from the neurotoxic compound HD. AcHD did not cross-link proteins in vitro. Pyrrole derivatives were demonstrated on hemoglobin isolated from animals treated with HD, DMHD, and AcHD. Cross-linked spectrin was detected in animals treated with HD and DMHD but not with AcHD. Rats receiving 0.1 or 0.25 mmol of AcHD/kg/day did not reach the end point of hindlimb paralysis observed in the gamma-diketone neuropathies, and the NF-filled axonal swellings seen following exposure to the neurotoxic gamma-diketones were not observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Electron microscopy and L-dopa reaction in the evaluation of an unusual amelanotic malignant melanoma of the neck.

A 28-year-old white man with a neck mass is described. A diagnosis of amelanotic melanoma was made by L-dopa reaction and electron microscopy. This tumor could represent a metastasis from an unknown primary or a primary that had undergone spontaneous regression. It could also be a rare primary tumor of the cervical sympathetic chain. Electron microscopy and the L-dopa reaction are emphasized as important adjuncts in the diagnoses of amelanotic melanoma.

Adult↗
PubMedDate not supplied

Ultrastructural morphometric data of human spermatozoa.

A morphometric study of the volumetric parameters of human spermatozoa has been carried out, volume densities being obtained by point counting and converted to absolute volumes by employing the point-sampled intercept method. Data for the Spermatozoa from the semen of 15 recently fertile men are presented. The significance of the results is discussed in relation to results obtained by other methods and in relation to the building of a diagnostic reference database.

Humans↗
PubMedDate not supplied

Hematuria associated with ruptured abdominal aortic aneurysms.

A retrospective study of the Staten Island University Hospital experience with ruptured abdominal aortic aneurysms (AAA) was undertaken. The study covered a 58 month period and included 30 patients. The purpose of the study was to investigate the relationship of ruptured AAA with hematuria. We specifically investigated (1) the incidence of hematuria in patients with ruptured AAA, (2) weather the presence of hematuria in these patients led to a delay in the diagnosis of ruptured AAA, and (3) if the presence of hematuria adversely effected survival as a function of causing a delay in diagnosis. The data revealed an 87% incidence of hematuria in ruptured AAA. Furthermore, gross hematuria was found to cause a statistically significant delay in arriving at the diagnosis of a ruptured AAA. This delay however could not be demonstrated to adversely affect patient survival.

Aged↗