Prevalence of Hepatitis δ (Delta) Virus Infection A Seroepidemiologic Study

In assessing the prevalence of hepatitis δ (delta) virus (HDV) infection in 358 patients with acute hepatitis B seen in Los Angeles between 1983 and 1985 and in 196 patients with chronic hepatitis B followed between 1980 and 1985, we found that 23% of patients with chronic and 5% of patients with acute hepatitis B were infected with HDV. Among patients with chronic hepatitis B, the prevalence of HDV infection was 73% in intravenous drug users and 14% in homosexual men. Acute coinfection with the hepatitis B virus was also more frequent in drug users (8%) than in other groups. δ-Hepatitis is a common infection in hepatitis B virus carriers in Los Angeles, particularly in drug addicts, but also in homosexual men who do not abuse drugs intravenously.     

ECOPHYSIOLOGY OF TROPICAL RHODOPHYTES. I. MICROSCALE ACCLIMATION IN PIGMENTATION1,2

Microscale pigment adjustments to a tropical photosynthetically active radiation and ultraviolet (UV) environment by the intertidal turf algae Ahnfeltiopsis concinna (J. Ag.) Silva et DeCew and Laurencia mcdermidiae (J. Ag) Abbott were promoted by thalli densities that self-shade the under story portions of the same diminutive axes. Tissues of A. concinna from canopy microsites had significantly reduced levels of phycoerythrin, phycocyanin, and allophycocyanin compared to tissues from understory microsites of the same axes. Tissues of L. mcdermidiae from canopy microsites had reduced levels of only phycoerythrin compared to tissues from understory microsites. These alterations coupled with enhanced levels of carotenoid and UV-absorbing compounds in tissues from canopy compared to tissues from understory microsites indicated a pattern of remarkably sensitive photoacclimation over the ≤10-cm axes of these turf-forming rhodophytes. Microscale variation in the in vivo UV absorbance capabilities for turfs of A. concinna and L. mcdermidiae was directly related to the amount of extractable UV-absorbing compounds. An in vivo absorbance signature at ～345 nm appears to provide a method to quickly and accurately gauge the potential UV-shielding capacity of primary producers even at remarkably fine ecological scales. The capacity for highly responsive biochemical adjustments that result in marked canopy–understory distinctions coupled with a turf morphology may be crucial for macroalgal tolerance of physiological stresses associated with tropical intertidal zones. This responsive capacity allows for enhanced photoprotective mechanisms in tissues from canopy microsites while optimizing irradiance capture in deeply shaded tissues from understory microsites < 10 cm away.     

Back Diffusion of Hydrogen Ions across Gastric Mucosa of Patients with Gastric Ulcer and Rheumatoid Arthritis

Ionic permeability of the gastric mucosa was measured in six patients with an acute exacerbation of severe generalized rheumatoid arthritis receiving either aspirin and prednisone or aspirin and indomethacin as therapy. The results were compared with those in four patients with benign gastric ulcer and nine normal subjects. Compared with controls H⁺ concentration was decreased and Na⁺ concentration increased while corrected H⁺ flux out of the lumen and Na⁺ flux into the lumen were significantly increased in the patient groups, indicating increased mucosal permeability. Abnormality of the gastric mucosal barrier persisted in two patients despite healing of their ulcers. Mucosal permeability of patients with rheumatoid arthritis and gastric ulcer did not differ significantly from one another. One rheumatoid patient with a gastric ulcer showed no difference in mucosal permeability to that of the other rheumatoid patients. These studies suggest that increased H⁺ ion loss contributes to the apparent hyposecretion of acid in patients gastric ulcer; persistence of an abnormal gastric mucosal barrier to H⁺ ions may explain the high recurrence rate of gastric ulcers; and an abnormal gastric mucosal barrier may be a precursor to gastric ulceration in rheumatoid arthritis.     

QuiC2 represents a functionally distinct class of dehydroshikimate dehydratases identified in Listeria species including Listeria monocytogenes

Many Listeria species including L. monocytogenes contain the pathway for the biosynthesis of protocatechuate from shikimate and quinate. The qui1 and qui2 operons within these Listeria spp. encode enzymes for this pathway. The diversion of shikimate pathway intermediates in some Listeria species to produce protocatechuate suggests an important biological role for this compound to these organisms. A total of seven ORFs, including quiC2, were identified within qui1 and qui2, however only three proteins encoded by the operons have been functionally annotated. The final step in Listeria's protocatechuate biosynthesis involves the conversion of dehydroshikimate by a dehydroshikimate dehydratase (DSD). In this study, we demonstrate that QuiC2 functions as a DSD in Listeria spp. through biochemical and structural analyses. Moreover, we show that QuiC2 forms a phylogenetic cluster distinct from other functionally annotated DSDs. The individual phylogenetic clusters of DSD are represented by enzymes that produce protocatechuate for distinct biological processes. Similarly, QuiC2 is expected to produce protocatechuate for a novel biological process. We postulate that protocatechuate produced by DSDs found within the QuiC2 phylogenetic cluster provides an ecological niche for representative organisms.     

Does phenotypic plasticity initiate developmental bias?

The generation of variation is paramount for the action of natural selection. Although biologists are now moving beyond the idea that random mutation provides the sole source of variation for adaptive evolution, we still assume that variation occurs randomly. In this review, we discuss an alternative view for how phenotypic plasticity, which has become well accepted as a source of phenotypic variation within evolutionary biology, can generate nonrandom variation. Although phenotypic plasticity is often defined as a property of a genotype, we argue that it needs to be considered more explicitly as a property of developmental systems involving more than the genotype. We provide examples of where plasticity could be initiating developmental bias, either through direct active responses to similar stimuli across populations or as the result of programmed variation within developmental systems. Such biased variation can echo past adaptations that reflect the evolutionary history of a lineage but can also serve to initiate evolution when environments change. Such adaptive programs can remain latent for millions of years and allow development to harbor an array of complex adaptations that can initiate new bouts of evolution. Specifically, we address how ideas such as the flexible stem hypothesis and cryptic genetic variation overlap, how modularity among traits can direct the outcomes of plasticity, and how the structure of developmental signaling pathways is limited to a few outcomes. We highlight key questions throughout and conclude by providing suggestions for future research that can address how plasticity initiates and harbors developmental bias.     

No support for the emergence of lichens prior to the evolution of vascular plants

The early‐successional status of lichens in modern terrestrial ecosystems, together with the role lichen‐mediated weathering plays in the carbon cycle, have contributed to the long and widely held assumption that lichens occupied early terrestrial ecosystems prior to the evolution of vascular plants and drove global change during this time. Their poor preservation potential and the classification of ambiguous fossils as lichens or other fungal–algal associations have further reinforced this view. As unambiguous fossil data are lacking to demonstrate the presence of lichens prior to vascular plants, we utilize an alternate approach to assess their historic presence in early terrestrial ecosystems. Here, we analyze new time‐calibrated phylogenies of ascomycete fungi and chlorophytan algae, that intensively sample lineages with lichen symbionts. Age estimates for several interacting clades show broad congruence and demonstrate that fungal origins of lichenization postdate the earliest tracheophytes. Coupled with the absence of unambiguous fossil data, our work finds no support for lichens having mediated global change during the Neoproterozoic‐early Paleozoic prior to vascular plants. We conclude by discussing our findings in the context of Neoproterozoic‐Paleozoic terrestrial ecosystem evolution and the paleoecological context in which vascular plants evolved.