THE ROLE OF LOCATION IN EVALUATING RACIAL WAGE DISPARITY.

A standard object of empirical analysis in labor economics is a modified Mincer wage function in which an individual's log wage is specified to be a function of education, experience, and an indicator variable identifying race. We analyze this approach in a context in which individuals live and work in different locations (and thus face different housing prices and wages). Our model provides a justification for the traditional approach, but with the important caveat that the regression should include location-specific fixed effects. Empirical analyses of men in U.S. labor markets demonstrate that failure to condition on location causes us to (i) overstate the decline in black-white wage disparity over the past 60 years, and (ii) understate racial and ethnic wage gaps that remain after taking into account measured cognitive skill differences that emerge when workers are young.

Are Children "Normal"?

We examine Becker's (1960) contention that children are "normal." For the cross section of non-Hispanic white married couples in the U.S., we show that when we restrict comparisons to similarly-educated women living in similarly-expensive locations, completed fertility is positively correlated with the husband's income. The empirical evidence is consistent with children being "normal." In an effort to show causal effects, we analyze the localized impact on fertility of the mid-1970s increase in world energy prices - an exogenous shock that substantially increased men's incomes in the Appalachian coal-mining region. Empirical evidence for that population indicates that fertility increases in men's income.

Extracellular regulated kinase/mitogen activated protein kinase is up-regulated in pulmonary emphysema and mediates matrix metalloproteinase-1 induction by cigarette smoke.

The interstitial collagenase matrix metalloprotein-ase-1 (MMP-1) is up-regulated in the lung during pulmonary emphysema. The mechanisms underlying this aberrant expression are poorly understood. Although cigarette smoking is the predominant cause of emphysema, only 15-20% of smokers develop the disease. To define the signaling pathways activated by smoke and to identify molecules responsible for emphysema-associated MMP-1 expression, we performed several in vitro and in vivo experiments. In this study, we showed that cigarette smoke directly induced MMP-1 mRNA and protein expression and increased the collagenolytic activity of human airway cells. Treatment with various chemical kinase inhibitors revealed that this response was dependent on the extracellular regulated kinase-1/2 (ERK) mitogen activated protein kinase pathway. Cigarette smoke increased phosphorylation of residues Thr-202 and Tyr-204 of ERK in airway lining cells and alveolar macrophages in mice at 10 days and 6 months of exposure. Moreover, analysis of lung tissues from emphysema patients revealed significantly increased ERK activity compared with lungs of control subjects. This ERK activity was evident in airway lining and alveolar cells. The identification of active ERK in the lungs of emphysema patients and the finding that induction of MMP-1 by cigarette smoke in pulmonary epithelial cells is ERK-dependent reveal a molecular mechanism and potential therapeutic target for excessive matrix remodeling in smokers who develop emphysema.

Expression of c-Met proto-oncogene in metastatic macrophage x melanoma fusion hybrids: implication of its possible role in MSH-induced motility.

It was shown previously that a majority of hybrids produced by in vitro fusion of normal macrophages with Cloudman S91 melanoma cells displayed macrophage-specific glycosylation, especially increased GnT-V activity, beta1,6 branch formation in glycoproteins, accompanied by enhanced metastatic potential in vivo and motility in vitro. These hybrids also express upregulated melanocortin-1 receptor (MC1-R) activity and exhibit increased motility after melanocyte-stimulating hormone (MSH) treatment. In this report, we show that MSH-mediated stimulation of motility is mediated through enhanced expression of c-Met proto-oncogene. In metastatic hybrids c-Met expression is induced by MSH, and addition of c-Met neutralizing antibody to cells inhibits MSH-induced motility but not the basal motility of the cells. Furthermore, abrogation of the chemoattractant gradient concentration by addition of hepatocyte growth factor (HGF) recombinant protein, a cognate ligand of c-Met receptor, reduces the MSH-induced effect on motility. A similar result was also obtained by the addition of blocking anti-alphaHGF antibody in the chemoattractant chamber. Again, the metastatic hybrids, but not the nonmetastatic hybrids or parental melanoma cells, showed significant motile response to rHGF chemoattractant, and that motility is further induced when cells were stimulated with MSH/isobutylmethyl xanthine (IBMX). Synergistic stimulation on motility was also observed with those hybrids treated with MSH/IBMX and when rHGF and fibronectin (FN), in combination, were used as chemoattractants. These indicate that MSH/IBMX-induced motility might involve c-Met pathways as well as extracellular matrix (ECM)/integrin pathways in a cooperative fashion. Ets-1, a transcription factor involved in the expression of c-Met, is also found to be induced in metastatic hybrids after exposure to MSH/IBMX. Implication of the result is discussed in light of the role of c-Met and its interacting proteins in the development of metastatic phenotypes and its therapeutic intervention.

Current Views on the Role of Neutrophil Granulocyte System.

At present there is no doubt concerning the capability of neutrophil granulocytes for cooperative interaction with other immunocompetent cells and substances of different nature, which as a whole provides a wide variety of forms of interaction and makes it possible for neutrophils to occupy key positions in the regulation of the functions of other cells both by direct contact and by secretion of regulatory mediators - neutrophilokines. Neutrophils realize their functional capabilities on a background of stimulating actions in the form of intensification of migrational, adhesive capability, readjustment of metabolism for activation of phagocytic and secretory function. It is also known that many cytokines support the viability of neutrophils, preventing their apoptosis, progressing proportional to the degree of severity of the purulent-septic process. The cytokine-producing function of the neutrophils is thereby necessary for the autocrine and paracrine regulating interaction of neutrophils with surrounding cells. Together with the established role of neutrophils during inflammatory infectious processes, their capability of expressed cytotoxic action in respect to foreign and pathologically changed cells is also known. Data on a study of the neutrophil system in healthy and sick subjects provides the possibility to consider them as the main effector cells of not only inflammatory protective reactions of the organism, but also as functionally relevant effector and regulatory structural units in the case of many other forms of immune protection of the organism against viruses, bacteria, protozoa, alloantigens, allergens both at the general and at the local level.