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Biomedical subjects

K M Campbell

Publications and source records attributed to K M Campbell.

16 recordsLinked to original sources
PubMed1997

Agonist activation of delta-opioid receptor but not mu-opioid receptor potentiates fetal calf serum or tyrosine kinase receptor-mediated cell proliferation in a cell-line-specific manner.

Activation by opioid receptors of cell proliferation was examined with fibroblast cell lines stably expressing either delta-opioid or mu-opioid receptors. Addition of [D-Ala2, D-Leu5]-enkephalin or [D-Pen2,D-Pen5]-enkephalin to Chinese hamster ovary (CHO) cells transfected with delta-opioid receptor cDNA resulted in an agonist concentration-dependent potentiation of fetal calf serum (FCS)-stimulated cell proliferation. This potentiation by delta-opioid agonists was antagonized by naloxone and was not observed with the kappa-opioid receptor selective agonist U50,488 or the mu-opioid receptor selective agonist [D-Ala2,N-MePhe4, Gly-ol5]-enkephalin. This delta-opioid agonist effect was not observed at FCS concentrations > 0.1% and could be blocked by pretreating cells with pertussis toxin, indicating that Gi/Go were involved in this action. In addition, delta-opioid agonists could potentiate CHO cell proliferation stimulated by those growth factors that are mediated by tyrosine kinase receptors (i.e., insulin, insulin-like growth factor 1, and fibroblast-derived growth factor b). This delta-opioid agonist potentiation of growth apparently was dependent on the level of delta-opioid receptors that were expressed and had cell-line selectivity. Activation of delta-opioid receptors expressed in Rat-1 or NIH3T3 fibroblast did not result in a modulation of the cell growth induced by FCS or by growth factors. Interestingly, in CHO cells transfected with mu-opioid receptor cDNA, activation with agonists did not produce a potentiation of FCS-stimulated proliferation. This lack of mu-opioid receptor effect was not due to the differences among CHO clones. In a CHO cell line transfected with both delta-opioid receptor cDNA and mu-opioid receptor cDNA, activation of delta-but not mu-opioid receptors resulted in a potentiation of growth. These data suggest that delta- and mu-opioid receptors in CHO cells activate similar but divergent second messenger pathways, resulting in the differential regulation of cell growth.

3T3 Cells↗
PubMed1991

Delirium after cessation of glucocorticoid therapy.

We report here a case of delirium that occurred after discontinuation of glucocorticoid therapy. Administration of hydrocortisone reversed the mental status changes seen in this patient. We review similar reported cases and discuss the direct actions of glucocorticoids on the brain.

Delirium↗
PubMed1990

Identification of Staphylococcus aureus binding proteins on isolated porcine cardiac valve cells.

Infective endocarditis caused by Staphylococcus aureus may be initiated by bacterial binding to cardiac valve cells. We investigated binding of whole S. aureus organisms to preparations of isolated porcine cardiac valve proteins. Cultured endothelial and subendothelial cells were surface labeled with iodine 125. After preabsorption with Escherichia coli, an organism that only rarely causes infective endocarditis, binding of surface proteins to S. aureus was assessed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and subsequent autoradiography. The results showed that cardiac valve endothelial cells expressed a major S. aureus-binding protein with an approximate apparent molecular weight of 120,000. In contrast, cardiac valve subendothelial cells expressed on their surface a single species of binding protein with an approximate apparent molecular weight of 220,000; immunoblot analysis suggested that this protein was fibronectin. We also used radiolabeled S. aureus to probe cellular proteins transferred to nitrocellulose membranes. This technique identified a 125,000 molecular weight protein that bound S. aureus in endothelial cell extracts. We conclude that specific S. aureus binding to cardiac valve cells is mediated by different receptors for endothelial and subendothelial cells.

Animals↗
PubMed1985

Bacteriophage T4 regA protein. Purification of a translational repressor.

The bacteriophage T4 regA protein translationally regulates its own synthesis and the synthesis of several other T4 early proteins. In order to study the mechanism of translational regulation, we have purified the regA protein. Initially a mutant protein, incapable of autogenous repression, was placed under lambda PL transcriptional control and amplified to approximately 10% of total cell protein. The membrane-associated mutant protein was extracted with organic solvent mixtures and purified by reverse phase-high performance liquid chromatography. Polyclonal antibodies prepared against the mutant protein were used in Western blot assays to monitor purification of the wild-type protein from T4-infected cells. Phosphocellulose and poly(U)-agarose chromatography were important steps in its purification. The binding properties of regA protein to polyribonucleotides are discussed in relation to the mechanism by which the protein recognizes its mRNA targets.

Amino Acid Sequence↗
PubMed1982

Revertants of a streptomycin-resistant, oligosporogenous mutant of Bacillus subtilis.

Revertants of a streptomycin-resistant (Strr), oligosporogenous (Spo-) mutant of Bacillus subtilis were selected form the ability to sporulate. The revertants obtained fell into two phenotypic classes: Strs Spo+ (streptomycin-sensitive, sporeforming), which arose by reversion of the streptomycin resistance mutations of the parent strain; and Strr Spo+, which arose by the acquisition of additional mutations, some of which were shown to affect ribosomal proteins. Alterations of ribosomal proteins S4 and S16 in the 30S subunit and L18 inthe 50S subunit were detected in Strr Spo+ revertants by polyacrylamide gel electrophoresis. Streptomycin resistance of the parental strain and the Strr revertants was demonstrated to reside in the 30S ribosomal subunit. The second site mutations of the revertants depressed the level of streptomycin resistance in vivo and in the in vitro translation of phage SP01 messenger ribonucleic acid (mRNA) relative to the resistance exhibited by the Strr parental strain. The Strr parent grew slowly and sporulated at approximately 1% of the wild type level. The Strr revertants closely resembled the wild type strain with regard to growth and sporulation. The Strr revertants grew at rates intermediate between those of the Strr patent and wild type, and sporulated at wild type levels.

Bacillus subtilis↗
PubMed1977

Streptomycin-resistant, asporogenous mutant of Bacillus subtilis.

A streptomycin-resistant mutantant of Bacillus subtilis that is also asporogenous, was isolated and partially characterized. This strain, SRB15, sporulated at a frequency of about 1% compared to the wild type frequency of greater than 70%. The two phenotypes were inseparable by transformation, suggesting that this strain carries a single mutation that causes it to be both streptomycin-resistant and spore-minus. The mutation cotransduces with cysA, the closest auxotrophic marker to the "ribosomal region" of the B. subtilis chromosome, with a frequency of 68%. SRB15 showed no cross resistence to other antiobiotics tested, including the aminoglycosides kanamycin, neomycin and spectinomycin. Ribosomes obtained from the mutant were at least 200-fold more resistant in vitro to streptomycin than were wild type ribosomes in the translation of phage SPO1 RNA. The kinetics of in vitro translation of this natural message were indistinguishable for mutant and wild type ribosomes. The level of misreading, as measured by poly(U)-directed isoleucine incorporation, by mutant ribosomes was less than that by wild type ribosomes.

Bacillus subtilis↗
PubMed1977

Pigmentation and musculoskeletal abnormalities in an aged state hospital population.

In a State hospital population, 686 patients (mean age, 65 years) were examined for patterned pigmentation on unexposed areas of the body. Of these patients, 285 (41.5 percent) met the criteria for pigmentation. There were no sex or age differences. Psychosis had been diagnosed in 96 percent of the pigmented group. All of the 239 patients examined orthopedically had vertebral malalignment greater than 15 degrees and often had other bony deformities. Nearly all of the pigmented group displayed dyskinetic activity. A possible mechanism for the production of the pigmentation-psychosis-skeletal deformity triad could be an alteration in the concentration of available melatonin. Continued research along these lines may lead to an effective means of pharmacologic treatment as well as better psychologic and physical care.

Adult↗