A computer model for reshaping of cells in epithelia due to in-plane deformation and annealing

Although cell reshaping is fundamental to the mechanics of epithelia, technical barriers have prevented the methods of mechanics from being used to investigate it. These barriers have recently been overcome by the cell-based finite element formulation of Chen and Brodland. Here, parameters to describe the fabric of an epithelium in terms of cell shape and orientation and cell edge density are defined. Then, rectangular "patches" of model epithelia having various initial fabric parameters are generated and are either allowed to anneal or are subjected to one of several patterns of in-plane deformation. The simulations show that cell reshaping lags the deformation history, that it is allayed by cell rearrangement and that it causes the epithelium as a whole to exhibit viscoelastic mechanical properties. Equations to describe changes in cell shape due to annealing and in-plane deformation are presented.     

Computer simulations of mitosis and interdependencies between mitosis orientation, cell shape and epithelia reshaping

Finite element-based computer simulations are used to investigate mitosis and how mitosis, cell shape, and epithelium reshaping depend on each other. Frame- and cell-oriented patterns of mitosis with growing and non-growing daughter cells are considered. Previous simulations have shown that applied stresses or strains can reshape cells so that their long axes are aligned in the principal stretch direction. The simulations reported here show that this can produce global alignment of the mitosis cleavage planes. Other simulations reported here show that mitoses with suitably aligned cleavage planes can drive epithelium reshaping. Formulas that quantify these and other dependencies are derived. These formulas provide quantitative relationships against which current hypotheses regarding epithelia reshaping in real biological systems can be evaluated.     

Mechanisms underlying in vivo neuroprotection by the endocannabinoid anandamide and the cannabinoid/vanilloid receptor agonist,arvanil

The endocannabinoid anandamide (AEA) and some of its oxidative metabolites are putative ligands for the vanilloid receptor (VR₁). AEA affords protection against excitotoxicity induced in vivo by ouabain, a Na⁺/K⁺‐ATPase inhibitor. This effect is only partly dependent of the cannabinoid CB₁ receptor. Here, we assessed whether VR₁ is involved in neuroprotection by AEA and arvanil, which is a hydrolysis‐stable ligand for both VR₁ and CB₁. Using magnetic resonance imaging we show that: (i) modulation of VR₁, by the agonists arvanil and capsaicin and the antagonist capsazepine, leads to neuroprotective effects in the late but not acute phase after i.c. ouabain‐injection; (ii) arvanil is a potent neuroprotectant, acting at both CB₁ and VR₁; and (iii) the neuroprotective effects of AEA are mediated by CB₁ but not by lipoxygenase metabolites or VR₁.     

Combined Review: Experiencing the New Genetics: Family and Kinship on the Medical Frontier and Born and Bred: Idioms and New Reproductive Technologies in England

Experiencing the New Genetics: Family and Kinship on the Medical Frontier. Kaja Finkler. Philadelphia: University of Pennsylvania Press, 2000. 296 pp.
Born and Bred: Idioms and New Reproductive Technologies in England. Jeanette Edwards. New York: Oxford University Press, 2000. 264 pp.     

Gene and domain duplication in the chordate Otx gene family: insights from amphioxus Otx

We report the genomic organization and deduced protein sequence of a cephalochordate member of the Otx homeobox gene family (AmphiOtx) and show its probable single-copy state in the genome. We also present molecular phylogenetic analysis indicating that there was single ancestral Otx gene in the first chordates which was duplicated in the vertebrate lineage after it had split from the lineage leading to the cephalochordates. Duplication of a C-terminal protein domain has occurred specifically in the vertebrate lineage, strengthening the case for a single Otx gene in an ancestral chordate whose gene structure has been retained in an extant cephalochordate. Comparative analysis of protein sequences and published gene expression patterns suggest that the ancestral chordate Otx gene had roles in patterning the anterior mesendoderm and central nervous system. These roles were elaborated following Otx gene duplication in vertebrates, accompanied by regulatory and structural divergence, particularly of Otx1 descendant genes.      

Regulation of ovarian ornithine decarboxylase: Role of calcium ions in enzyme induction in isolated swine granulosa cells in vitro

When swine granulosa cells were cultured in chemically defined medium selectively deficient in Ca²⁺, the dose-dependent stimulation of ornithine decarboxylase (EC 4.1.1.17) activity in response to prostaglandin E₂, l-epinephrine or the somatomedin, multiplication-stimulating activity, was attenuated markedly. Putative calcium influx blockers, verapamil and diltiazem, also inhibited hormone-stimulated enzymic activity. Similar inhibitory effects were exerted by divalent (cobalt) or trivalent (lanthanum) cations believed to compete with calcium for extracellular binding sites. The suppressive effects of extracellular calcium deprivation were time-dependent (suggesting gradual depletion of intracellular calcium stores), and could be mimicked by the intracellular antagonist of calcium action, trifluoperazine. The mechanism(s) subserving diminished hormonal induction of enzyme activity could not be accounted for by alterations in cell viability, general protein synthesis, half-life of decay of enzyme activity (measured in the presence of cycloheximide), or apparent K_m of ornithine decarboxylase. Ca²⁺ and/or calcium antagonists did not modify enzyme activity in cell-free preparations. These observations implicate Ca²⁺ in the hormonal induction of a discrete cytosolic enzyme in isolated intact ovarian cells.     

First Record of Rosellinia desmazieresii on Scots Pine and its Association with Disease in Poland

Rosellinia desmazieresii was found for the first time on a tree of Scots pine. It occurred on a dying tree in a mixed Scots pine-oak plantation in Poland. The fungus girdled the base of the trunk, where perithecia were produced abundantly. The fungus was evidently the cause of the tree's poor growth and ultimate death.