What happens at the molecular level when two surfaces, held together by an adhesive film, are pulled apart? The answer depends on the type and state of the adhesive, the temperature, the speed at which the surfaces are pulled apart, and the strength of bonding between the surfaces and the adhesive. Entangled adhesive molecules resist rupture, leading to a buildup of energy that is dissipated differently, depending on the state of the polymer. Baljon and Robbins (p. p. 482) performed molecular dynamics calculations to follow individual polymer changes during this process, and have identified three mechanisms of energy dissipation during rupture that have parallels to macroscopic phenomena observed in commercial adhesives.
Materials that contain chain structures can approximate one-dimensional systems, whose properties, such as the magnetic coupling between electrons, can be quite different from that seen in three-dimensional systems. Nguyen et al. (p. 489) describe a compound, Sr3CuPt0.5Ir0.5O6, that is a solid solution of ferromagnetic Sr3CuPtO6 and antiferromagnetic Sr3CuIrO6. This intermediate compound forms a random quantum spin chain paramagnet—the coupling of spins along the chain through exchange interactions can be randomly ferromagnetic or antiferromagnetic.
Enzyme clocks for kingdom divergence
Most mutations in proteins occur as random events over time, so, in principle, one can estimate when divergence occurred from a common ancestor by analyzing sequences of the same protein from different organisms. In practice, proteins mutate at different rates, and functionally similar proteins may in fact have different origins. Doolittle et al. ( p. 470; see the news story by Morell, p. 448) analyzed divergence times for 57 different enzymes from organisms from all of the major biological groups. The analysis of this large data set indicates that eukaryotes and eubacteria had a common ancestor about 2 billion years ago, or about twice as long ago as the plant-animal divergence.
Linking atmospheric oxygen and phosphorus
Oxygen levels in Earth's atmosphere evidently have been maintained at levels that allow life to persist for billions of years. The controls that essentially buffer the system have been uncertain. Van Cappellen and Ingall (p. 493; see the Perspective by Kump and Mackenzie, p. 459) suggest that the key is the phosphorus cycle; phosphorus is a key nutrient driving oceanic production and respiration, is a minor component of the atmosphere, and its burial is extremely sensitive to the oxidation state of the oceans. Analysis of phosphorus burial in the past shows that when waters are low in oxygen, less phosphorus is buried.
During the first few weeks of HIV infection, the concentration of virus in plasma rises but then drops off. Phillips ( p. 497) has modeled the course of early HIV infection and suggests that the drop-off is not an HIV-specific immune response but is actually due to population dynamics in HIV replication. The supply of uninfected cells is quickly depleted, thus decreasing virus production.
Although the DNA sequence of an ancestral gene may be predictable, the enzymatic function of the protein product may not be. Chandrasekharan et al. (p. 502) used extant chymase gene sequences to predict the ancestral form of the enzyme, and then expressed the enzyme and characterized its kinetics for converting angiotensin I to angiotensin II. The ancestral form is very specific and efficient for this reaction, and some modern chymases actually have less substrate specificity than this ancestral form.
Hepatitis G virus
In some hepatitis cases, the causative agent is unknown, which suggests that some hepatitis viruses are still unidentified. Linnen et al. (p. 505) identified an RNA virus, hepatitis G virus (HGV), by analyzing immunoreactive complementary DNA clones from a patient who was also infected with hepatitis C virus. Although the pathogenesis of HGV remains to be determined, it is associated with both acute and chronic hepatitis and is present in the blood-donor population.
About 20 to 25% of patients with familial amyotrophic lateral sclerosis (FALS) have mutations in the gene encoding copper-zinc superoxide dismutase (CuZnSOD). Wiedau-Pazos et al. (p. 515; see the news story by Marx, p. 446) show that the mutant CuZnSOD is more active than wild type in catalyzing oxidation of a model substrate, and that this enhanced activity can be inhibited by copper chelators. In a cell culture model of FALS, copper chelators inhibited the cell death induced by mutant CuZnSOD. Aberrant oxidative reactions catalyzed by mutant CuZnSOD may underlie the neuropathologic changes in FALS, and copper chelators may have therapeutic value for some FALS patients.
Programmed cell death (PCD), which typically occurs through apoptosis, is a normal function in multicellular organisms. Disregulated PCD, however, can cause numerous disorders, including neurodegenerative diseases and cancer. Several studies indicate that Ca2+ plays a role in apoptosis; Vito et al. (p. 521) developed a selection system which allowed them to identify two genes, ALG-2 and ALG-3, that mediate apoptosis. The ALG-2 gene encodes a Ca2+-binding protein required for several apoptotic pathways, and the ALG-3 gene is homologous to the Alzheimer's disease gene STM2.