Managed care: a call for strategic management in the dental office

Strategic management of any business will enable it to prosper in challenging times of change. Strategic planning is not characteristically found only in large corporations. Indeed, small business, such as solo private practices, can gain much from the process. The successful practice is one that is proactive rather than reactive; it has learned to become the beneficiary of change, rather than its victim.     

Chronic growth stimulation of human adult melanocytes by inflammatory mediators in vitro: implications for nevus formation and initial steps in melanocyte oncogenesis

In the human epidermis, melanocytes are distributed at a distance from each other. In contrast, melanocytes in nevi, which are considered benign neoplasms of melanocytes, are grouped in nests. Although still not well defined, environmental factors are thought to play an important role in the development of nevi. We found that chronic growth stimulation by leukotriene C4, a compound found in increased amounts in inflamed skin, induced pleiotropic modifications in the normal melanocyte phenotype. These changes include loss of contact inhibition and formation of structures resembling tumor spheroids. In parallel with these changes, there was a constitutive expression of Fos protein. Switching these cultures to medium supplemented with phorbol ester sustained growth with reversion of the altered phenotype. In contrast, a cAMP stimulator, cholera toxin, induced features of terminal differentiation. Our findings suggest a role for inflammatory mediators in human epidermal melanocytes. This observation provides insight into melanocyte growth alterations which may have relevance in early stages of melanocyte oncogenesis.     

Linkage analysis in familial Alzheimer disease: description of the Duke and Boston data sets

Familial Alzheimer diseases is a neurological disorder of adult onset. Three research centers have each contributed their families and genetic linkage data for combined analyses. The data from the Duke and Boston centers, comprising 73 pedigrees for whom numerous markers on chromosomes 19 and 21 were typed are described.     

Inferior vena cava filters in cancer patients: indications and outcome

Estrogen, like other steroids, may induce rapid nongenomic cellular effects. We studied the effect on intracellular cAMP of short-term exposure (5 min) of cultured rat pulmonary vascular smooth muscle cells (VSMC) to estradiol 17 beta. At confluence, VSMC were incubated in phosphate buffer saline for 1 hr before exposure to different hormones. The reaction was stopped with 0.1 N HCl and cyclic adenosine monophosphate (cAMP) was measured by radioimmunoassay. The 5-min incubation with estradiol 17 beta (0.3-30 microM) significantly increased basal intracellular cAMP in a concentration-dependent manner. The stimulatory effect of estradiol on cAMP was time-dependent, increasing with prolonged exposure to the hormone, and was not affected by the protein synthesis inhibitor, actinomycin D (5 micrograms/ml), at 5 and 30 min. Comparable concentrations of testosterone or estradiol 17 alpha had no significant effect on cAMP. The estrogen receptor partial agonist, tamoxifen also significantly increased basal cAMP in a concentration-dependent manner, but inhibited the effect of estradiol. Furthermore, forskolin elicited a concentration-dependent increase in cAMP (396.6 +/- 53% at 10 microM concentration), which was significantly potentiated in presence of estradiol. The effect of estradiol is unlikely to be mediated by G-protein activation, because the G protein inhibitor, pertussis toxin (100 ng/ml), did not significantly affect estradiol-induced increase in cAMP. Removal of Ca++ from the incubation medium inhibited the stimulatory effect of estradiol 17 beta suggesting that estradiol may increase pulmonary VSMC cAMP via a Ca(++)-dependent pathway. We suggest that the effect of estradiol 17 beta in these experiments is nongenomic in nature, and is possibly mediated by direct interaction of the hormone with specific membrane binding sites.     

Further observations on enterovirus infection in specific-pathogen-free turkey poults

To evaluate sites of enterovirus replication and to characterize the resulting lesions, twenty 4-day-old specific-pathogen-free (SPF) turkey poults were orally inoculated with an enterovirus. Twenty uninoculated SPF poults served as controls. Inoculated poults were depressed, had ruffled feathers, watery droppings, and pasted vents. Gross lesions were dilated thin-walled ceca with foamy yellow fluid. Immune electron microscopy of the gastrointestinal tract contents revealed an enterovirus with an average diameter of 23.5 nm. Immunoperoxidase and indirect immunofluorescent antibody assays revealed intracytoplasmic staining in enterocytes of the duodenum, jejunum, and ileum. This correlated with the scanning electron microscopy findings, which showed the most lesions in the jejunum and ileum. The ileum had prominent cell outlines because of rounded, distinct, bulging epithelial cells. Histopathology revealed slight shortening of villi and increased crypt depth in the intestines of inoculated poults. Our findings indicate that the small intestine is the site of turkey enterovirus replication, and the gross and microscopic changes observed are determined to result from viral damage to the enterocytes.