The pace of modern life, revisited.

Wild populations must continuously respond to environmental changes or they risk extinction. Those responses can be measured as phenotypic rates of change, which can allow us to predict contemporary adaptive responses, some of which are evolutionary. About two decades ago, a database of phenotypic rates of change in wild populations was compiled. Since then, researchers have used (and expanded) this database to examine phenotypic responses to specific types of human disturbance. Here, we update the database by adding 5675 new estimates of phenotypic change. Using this newer version of the data base, now containing 7338 estimates of phenotypic change, we revisit the conclusions of four published articles. We then synthesize the expanded database to compare rates of change across different types of human disturbance. Analyses of this expanded database suggest that: (i) a small absolute difference in rates of change exists between human disturbed and natural populations, (ii) harvesting by humans results in higher rates of change than other types of disturbance, (iii) introduced populations have increased rates of change, and (iv) body size does not increase through time. Thus, findings from earlier analyses have largely held-up in analyses of our new database that encompass a much larger breadth of species, traits, and human disturbances. Lastly, we use new analyses to explore how various types of human disturbances affect rates of phenotypic change, and we call for this database to serve as a steppingstone for further analyses to understand patterns of contemporary phenotypic change.

CEACAM1 impedes thyroid cancer growth but promotes invasiveness: a putative mechanism for early metastases.

CEACAM1, also known as biliary glycoprotein (BGP), CD66a, pp120 and C-CAM1, is a member of the CEA immunoglobulin superfamily. CEACAM1 is a putative tumor suppressor based on diminished expression in some solid neoplasms such as colorectal carcinoma. However, CEACAM1 is overexpressed in some tumors such as non-small cell lung cancer. To clarify the mechanism of action of this cell adhesion molecule, we studied thyroid carcinoma that has a spectrum of morphologies and variable behavior allowing separation of proliferation from invasion and metastasis. CEACAM1 is expressed in thyroid carcinoma cell lines derived from tumors that exhibit aggressive behavior. Introduction of CEACAM1 into endogenously deficient WRO cells resulted in reduced cell cycle progression associated with p21 upregulation and diminished Rb phosphorylation. Forced CEACAM1 expression enhanced cell-matrix adhesion and migration and promoted tumor invasiveness. Conversely, small interfering RNA (siRNA)-mediated downregulation of CEACAM1 expression in MRO cells accelerated cell cycle progression and significantly enhanced tumor size in xenografted mice. CEACAM1 is not appreciably expressed in normal thyroid tissue or benign thyroid tumors. In a human thyroid tissue array, CEACAM1 reactivity was associated with metastatic spread but not with increased tumor size. These findings identify CEACAM1 as a unique mediator that restricts tumor growth whereas increasing metastatic potential. Our data highlight a complex repertoire of actions providing a putative mechanism underlying the spectrum of biologic behaviors associated with thyroid cancer.

Occurence of psychiatric disorder in a county jail population.

The authors report on a year's experience in providing psychiatric services in a county jail setting. Of 545 inmates evaluated, 22% were diagnosed as psychotic and 23% had a history of long-term or multiple hospitalizations. The authors discuss the implications of these data in terms of the problem of providing adequate psychiatric care for such a population.

B lymphocytes as emerging mediators of insulin resistance.

Obesity is associated with chronic inflammation of various tissues including visceral adipose tissue (VAT), which contributes to insulin resistance. T cells and macrophages infiltrate VAT in obesity and orchestrate this inflammation. Recently, we made the surprising discovery that B cells are important contributors to this process. Thus, some B cells and the antibodies they produce can promote VAT-associated and systemic inflammation, leading to insulin resistance. This report will focus on the properties of these B cells, and how they contribute to insulin resistance through T-cell modulation and production of pathogenic autoantibodies. Understanding the mechanisms by which B cells contribute to insulin resistance should lead to new antibody-based diagnostics and B-cell modulating therapeutics to manage this increasingly prevalent disease.