Cannon, Barbara, and Jan Nedergaard. Brown Adipose Tissue: Function and Physiological Significance. Physiol Rev 84: 277–359, 2004; 10.1152/physrev.00015.2003.—The function of brown adipose tissue i...

Brown Adipose Tissue: Function and Physiological Significance

Urbanization as a major cause of biotic homogenization

In the early 19th century, building on observations of microscopists now ancient, Schleiden and Schwann formulated the doctrine that cells are building blocks for plant and animal tissues (1). By the mid-19th century, Raspail, Remak, and Virchow expanded this hypothesis by suggesting that all cells come from preexisting cells — the so-called cell theory. Although referring to cell division, this now classic notion is prescient of another contemporary twist in the biology of cell maturation: beyond lineage development and normal differentiation, mature epithelial cells under new environmental pressures exhibit a local plasticity that allows them to morph into other mature phenotypes with or without proliferation (2, 3). Growing interest in the biology of these cellular transitions helped both establish epithelial cell plasticity as a field of study in the late 20th century and fashion much of the current thinking regarding morphogenesis in early embryonic development, tissue repair, and cancer metastasis (4–6). The details of some of these processes are not discussed here, as they are outlined in other articles in this Review Series on epithelial-mesenchymal transition (EMT) (7, 8). Instead, we offer a personal view gathered from our own experience and the literature regarding an approach documenting EMT events in culture or tissue. We hope this serves to stimulate other points of view as new data emerge.

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Biomarkers for epithelial-mesenchymal transitions

Many studies have described the effects of urbanization on species richness. These studies indicate that urbanization can increase or decrease species richness, depending on several variables. Some of these variables include: taxonomic group, spatial scale of analysis, and intensity of urbanization. Recent reviews of birds (the most-studied group) indicate that species richness decreases with increasing urbanization in most cases but produces no change or even increases richness in some studies. Here I expand beyond the bird studies by reviewing 105 studies on the effects of urbanization on the species richness of non-avian species: mammals, reptiles, amphibians, invertebrates and plants. For all groups, species richness tends to be reduced in areas with extreme urbanization (i.e., central urban core areas). However, the effects of moderate levels of urbanization (i.e., suburban areas) vary significantly among groups. Most of the plant studies (about 65%) indicate increasing species richness with moderate urbanization whereas only a minority of invertebrate studies (about 30%) and a very small minority of non-avian vertebrate studies (about 12%) show increasing species richness. Possible explanations for these results are discussed, including the importance of nonnative species importation, spatial heterogeneity, intermediate disturbance and scale as major factors influencing species richness.

Effects of urbanization on species richness: A review of plants and animals

Last Child in the Woods: Saving Our Children From Nature-Deficit Disorder

Currently, slightly less than half the world's population lives in dense urban areas, principally cities. In Australia, nearly 85% of people live in towns with 1000 or more residents. Although individual species of urban flora and fauna have often been well studied, little is known of the long-term temporal patterns associated with changes in both the abiotic and biotic environments as urban systems expand. Using historical and current information, the changes in species richness (defined as the native and introduced vertebrates and vascular plants) in Adelaide, South Australia, are described from its founding in 1836 until 2002. Adelaide is an isolated city of over a million inhabitants, bordered by a range of hills and the South Australian coastline. With a Mediterranean climate, a culture that places high importance on private residential gardens, and the presence of extensive public parklands, the metropolitan area has a significant diversity of both native and introduced flora and fauna. Using only the presence or absence of a species, the changes to plant and vertebrate species richness were quantified by analyzing the observed patterns of change at a functional group level. Powerful correlative evidence is provided to explain the development and establishment of patterns in urban ecology.

There has been a dramatic change in species composition, with an increase in total species numbers of ∼30%. At least 132 native species of plants and animals have become locally extinct, and a minimum of 648 introduced species have arrived (mostly plants). The plants increased in species richness by 46%. Fifty percent of the native mammal species were lost, and overall, the birds declined by one species, representing 21 extinctions and 20 successful introductions. Amphibians and reptiles showed no net change. The herbaceous perennial and annual plant species richness showed a substantial increase. This temporal approach to urban ecology demonstrates new ways to identify individual species or groups at risk of extinction and provides some long-term management goals for large urban areas.

Changes in species assemblages within the adelaide metropolitan area, australia, 1836–2002

Pulmonary surfactant controls the surface tension at the air-liquid interface within the lung. This system had a single evolutionary origin that predates the evolution of the vertebrates and lungs. The lipid composition of surfactant has been subjected to evolutionary selection pressures, particularly temperature, throughout the evolution of the vertebrates.

Pulmonary Surfactant: The Key to the Evolution of Air Breathing

Locomotor capacities and their physiological bases are thought to be of considerable selective importance in natural populations. Within this functional complex, organismal performance traits (e.g., speed, stamina) are expected to be of more direct selective importance than their suborganismal determinants (e.g., heart size). Quantitative genetics theory predicts that traits of greater selective importance should generally have lower heritabilities at equilibrium. Contrary to these expectations, we report that organismal performance traits had the highest heritabilities in a natural population of garter snakes.

Heritability of locomotor performance and its correlates in a natural population

In most eutherian mammals, cholesterol (Chol) comprises approximately 8-10 wt.% or 14-20 mol.% of both alveolar and lamellar body surfactant. It is regarded as an integral component of pulmonary surfactant, yet few studies have concentrated on its function or control. Throughout the evolution of the vertebrates, the contribution of cholesterol relative to surfactant phospholipids decreases, while that of the disaturated phospholipids (DSP) increases. Chol generally appears to dominate in animals with primitive bag-like lungs that lack septation, in the saccular lung of snakes or swimbladders which are not used predominantly for respiration, and also in immature lungs. It is possible that in these systems, cholesterol represents a protosurfactant. Cholesterol is controlled separately from the phospholipid (PL) component in surfactant. For example, in heterothermic mammals such as the fat-tailed dunnart, Sminthopsis crassicaudata, and the microchiropteran bat, Chalinolobus gouldii, and also in the lizard, Ctenophorus nuchalis, the relative amount of Chol increases in cold animals. During the late stages of embryonic development in chickens and lizards, the Chol to PL and Chol to DSP ratios decrease dramatically. While in isolated lizard lungs, adrenaline and acetylcholine stimulate the secretion of surfactant PL, Chol secretion remains unaffected. This is also supported in isolated cell studies of lizards and dunnarts. The rapid changes in the Chol to PL ratio in response to various physiological stimuli suggest that these two components have different turnover rates and may be packaged and processed differently. Infusion of [3H]cholesterol into the rat tail vein resulted in a large increase in Chol specific activity within 30 min in the lamellar body (LB) fraction, but over a 48-h period, failed to appear in the alveolar surfactant fraction. Analysis of the limiting membrane of the lamellar bodies revealed a high (76%) concentration of LB cholesterol. The majority of lamellar body Chol is, therefore, not released into the alveolar compartment, as the limiting membrane fuses with the cell membrane upon exocytosis. It appears unlikely, therefore, that lamellar bodies are the major source of alveolar Chol. It is possible that the majority of alveolar Chol is synthesised endogenously within the lung and stored independently from surfactant phospholipids. The role of cholesterol in the limiting membrane of the lamellar body may be to enable fast and easy processing by maintaining the membrane in a relatively fluid state.

The roles of cholesterol in pulmonary surfactant: insights from comparative and evolutionary studies.

Surface tension is reduced at the air–liquid interface in the lung by a mixture of lipids and proteins termed pulmonary surfactant. This study is the first to provide evidence for the presence of a surfactant-specific protein (Surfactant Protein A—SP-A) in the gas-holding structures of representatives of all the major vertebrate groups. Western blot analysis demonstrated cross-reactivity between an antihuman SP-A antibody and material lavaged from lungs or swimbladders of members from all vertebrate groups. Immunocytochemistry localized this SP-A–like protein to the air spaces of lungs from the actinopterygiian fish and lungfish. Northern blot analysis indicated that regions of the mouse SP-A cDNA sequence are complementary to lung mRNA from all species examined. The presence of an SP-A–like protein and SP-A mRNA in members of all the major vertebrate groups implies that the surfactant system had a single evolutionary origin in the vertebrates. Moreover, the evolution of the surfactant system must have been a prerequisite for the evolution of airbreathing. The presence of SP-A in the goldfish swimbladder demonstrates a role for the surfactant system in an organ that is no longer used for airbreathing.

Christopher B. Daniels

Papers

Changes in species assemblages within the adelaide metropolitan area, australia, 1836–2002

Pulmonary Surfactant: The Key to the Evolution of Air Breathing

Heritability of locomotor performance and its correlates in a natural population

The roles of cholesterol in pulmonary surfactant: insights from comparative and evolutionary studies.

Conservation of Surfactant Protein A: Evidence for a Single Origin for Vertebrate Pulmonary Surfactant