LISTA, LISTA-HOP and LISTA-HON: a comprehensive compilation of protein encoding sequences and its associated homology databases from the yeast Saccharomyces.

We continued our effort to make a comprehensive database (LISTA) for the yeast Saccharomyces cerevisiae. As in previous editions the genetic names are consistently associated to each sequence with a known and confirmed ORF. If necessary, synonyms are given in the case of allelic duplicated sequences. Although the first publication of a sequence gives-according to our rules-the genetic name of a gene, in some instances more commonly used names are given to avoid nomenclature problems and the use of ancient designations which are no longer used. In these cases the old designation is given as synonym. Thus sequences can be found either by the name or by synonyms given in LISTA. Each entry contains the genetic name, the mnemonic from the EMBL data bank, the codon bias, reference of the publication of the sequence, Chromosomal location as far as known, SWISSPROT and EMBL accession numbers. New entries will also contain the name from the systematic sequencing efforts. Since the release of LISTA4.1 we update the database continuously. To obtain more information on the included sequences, each entry has been screened against non-redundant nucleotide and protein data bank collections resulting in LISTA-HON and LISTA-HOP. This release includes reports from full Smith and Watermann peptide-level searches against a non-redundant protein sequence database. The LISTA data base can be linked to the associated data sets or to nucleotide and protein banks by the Sequence Retrieval System (SRS). The database is available by FTP and on World Wide Web.     

Dynamics of structural changes in the organs of immunity of rabbits with acute experimental appendicitis]

Cyto- and histological analysis of the whole immunogenic system at the development of an acute experimental appendicitis in rabbits has demonstrated that all the constituent parts of the system are involved into the reaction. In the central organ of immunity--thymus the main change is its progressive exhaustion, while peripheral organs of immunity are subjected to rather essential cytological rearrangements and activation of both cellular and humoral immunity. Accordingly to the type of the reaction, two groups of peripheral organs of immunity can be distinguish: the first--the appendix and the iliocecal lymph node which predominantly participate in the immunoblastic reaction and in the reaction of young plasmatic cells and demonstrate increased signs of immature cells emigration; the second--the axillary lymph node, as a representative of somatic nodes, and the spleen--the main carriers of the reaction in mature plasmic cells. Structural peculiarities of the complex appendix--iliocecal lymph node in intact animals and in the experiment make it possible to consider the complex as a peculiar functional link of the immune peripheral organs.     

Frequent and parallel habitat transitions as driver of unbounded radiations in the Cape flora

The enormous species richness in the Cape Floristic Region (CFR) of Southern Africa is the result of numerous radiations, but the temporal progression and possible mechanisms of these radiations are still poorly understood. Here, we explore the macroevolutionary dynamics of the Restionaceae, which include 340 species that are found in all vegetation types in the Cape flora and are ecologically dominant in fynbos. Using an almost complete (i.e., 98%) species‐level time calibrated phylogeny and models of diversification dynamics, we show that species diversification is constant through the Cenozoic, with no evidence of an acceleration with the onset of the modern winter‐wet climate, or a recent density‐dependent slowdown. Contrary to expectation, species inhabiting the oldest (montane) and most extensive (drylands) habitats did not undergo higher diversification rates than species in the younger (lowlands) and more restricted (wetland) habitats. We show that the rate of habitat transitions is more closely related to the speciation rate than to time, and that more than a quarter of all speciation events are associated with habitat transitions. This suggests that the unbounded Restionaceae diversification resulted from numerous, parallel, habitat shifts, rather than persistence in a habitat stimulating speciation. We speculate that this could be one of the mechanisms resulting in the hyperdiverse Cape flora.     

An unexpected by-product obtained during the preparation of technetium(III) boronic acid adducts of dioximes. The single crystal structure of TcCl(DMG)2(BDI)BEt (DMG=dimethylglyoxime, BDI=butane-2, 3-dione imine-oxime)

An unusual Tc(III) boron-capped imine-oxime complex has been isolated from the reaction of ⁹⁹TcCl₃(CH₃CN)(PPh₃)₂, dimethyl glyoxime (DMG) and ethyl boronic acid (EtB(OH)₂). A single crystal X-ray structure analysis of this molecule ⁹⁹TcCl(DMG)₂(BDI)BEt (BDI=butane-2, 3-dione imine-oxime) shows it to be seven coordinate: TcClC₁₄H₂₅N₆O₅B, a=9.073(2), b=23.686(5), c=19.539(6) Å; β=93.77(2)°, P2₁/n, Z=8. Its structure is very similar to that of previously reported Tc(III) complexes ⁹⁹TcCl(dioxime)₃BR, except that one dioxime ligand on the molecule has been reduced to an imineoxime.     

Abnormal glucocorticoid receptor gene and mRNA in primary cortisol resistance

Abnormal steroid hormone receptors have been implicated as causing several forms of primary steroid hormone resistance in humans, but as yet no abnormality has been described at the gene level. We describe the analysis of the mRNA and genomic DNA from the Epstein-Barr (EB) virus transformed cells of two siblings with Primary Cortisol Resistance. The cells of the propositus and his brother show a decreased level of glucocorticoid receptor (GR) mRNA, and the genomic DNA of both individuals shows an altered restriction enzyme pattern with the restriction enzyme Bgl II, one of eleven restriction enzymes tested. The genomic differences could be detected with a probe specific for the putative steroid binding domain of the human GR gene.