Electronic structure of Z+1 impurities in metals.
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Biomedical subjects
Publications and source records attributed to R Zeller.
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Models of marine ecosystem productivity rely on estimates of small-scale interactions, particularly those between copepods and their algal food sources. Rothschild and Osborn [Rothschild, B. J. & Osborn, T. R. (1988) J. Plankton Res. 10, 465-474], hypothesized that small-scale turbulence in aquatic systems increases the perceived abundance of prey to predators. We tested this hypothesis by exposing the planktonic copepod Centropages hamatus to turbulent and nonturbulent environments at different prey concentrations. Our results fell into two main categories. First, the response to turbulence was characterized by an initial period having a high number of escape reactions. This period was followed by one of increased foraging. C. hamatus responded to the higher encounter rates due to turbulence as if it were experiencing altered prey concentrations. Second, the termination of turbulence resulted in an increased foraging response, which was not directly related to the encounter rate. Functional response curves do not adequately explain this foraging response because the time course of the foraging response depends on prior encounter experience and foraging motivation.
In an effort to identify widely active positive regulatory elements, we have examined the action of the cytomegalovirus enhancer-promoter in transgenic mice. These elements activated expression in 24 of 28 tissues tested. The greatest expression was observed in the heart, kidney, brain, and testis. Maximum expression further localized to specific cells within the heart and kidney.
This is undoubtedly a rather rare clinical picture. The existence of a brain pressure syndrome with symptoms such as headache, increased cerebrospinal fluid pressure, and diplopia simulates a brain tumor, even though the radiological and tomographical evidence is absolutely normal. Therapeutic possibilities are steroid medication, lumbar punctions, as well as a neurosurgical intervention installing a lumboperitoneal drainage. We deem the initial dosage of 16 mg Millicorten/day to be therapeutically effective and adequate.
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To gain insight into the role of the limb deformity (ld) gene in limb morphogenesis, we examined the morphologic details of early embryonic limb formation in the mutant ld/ld mouse. Initial morphological differences between wild-type and homozygous ld embryos are apparent during early gestational day 10, a time period during which anteroposterior limb morphogenesis occurs. As a result of a shortened anteroposterior axis, the mutant limb bud appears more pointed than its wild-type counterpart. In addition, the apical ectodermal ridge (AER), a structure crucial to both proximodistal and anteroposterior limb development, fails to differentiate properly in mutant ld embryos. Consistent with these observations, molecular analysis of the limb promordia shows that the limb ectoderm contains a level of ld transcripts fivefold higher relative to its mesenchyme. Furthermore, expression of ld transcripts in other parts of the developing embryo and in primitive streak embryos (gestational day 7) suggests possible roles for this gene in the earliest determinative events of morphogenesis. These data lead us to conclude that ld gene products are required for both proper AER differentiation and anteroposterior pattern formation in limb mesenchyme.
The Pena-Shokeir syndrome is undoubtedly a rare clinical picture. The aim of this work is to introduce this syndrome, which was first described 14 years ago, and to show the (limited) possibilities of intrauterine diagnosis. The fact that the etiology of the Pena-Shokeir syndrome is still discussed indicates the necessity to expand our knowledge on this clinical entity.
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The first exon of the c-myc gene has unusual properties that suggest some further role in gene regulation. It encodes a large, evolutionarily conserved leader exon that is transcribed more frequently than the remaining exons of the c-myc gene. In what follows, we provide a possible explanation for these observations. We find that the major promoter of the c-myc gene is bifunctional; that is, it supports transcription by RNA polymerases II and III (pol II and III). Both enzymes initiate in vitro transcription from the major c-myc initiation site (P2), but pol III is completely blocked near the 3' end of the first exon while pol II, though partially blocked, transcribes through this region. These superimposed transcriptional activities suggest a potential regulatory mechanism by which one polymerase system could influence the activity of another.
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