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Biomedical subjects

D Schild

Publications and source records attributed to D Schild.

66 records · Page 4Linked to original sources
PubMed1984

Criteria for excitation and inhibition in peristimulus spike train activity.

Five possibilities of defining a coefficient of facilitation and inhibition are described. It is shown that the application of these definitions to the same spike train activity eventually leads to considerably different results, e.g., a response which is inhibitory according to one definition sometimes is facilitatory according to another definition. To find the most reliable definition the theoretical differences between the five alternatives are examined, whereby a coefficient is considered reliable if it is reproducible and independent of external experimental parameters, such as the record length. As an experimental example spike trains were recorded from mitral cells in the olfactory bulb of the goldfish. We divide every response into two sections: an initial reaction and a steady state reaction. In this way each response can be uniquely classified. The most reliable definition of a coefficient of facilitation turns out to be based on the steady state levels of an averaged peristimulus time histogramme. Under certain conditions this corresponds to considering the means of the sample mean rates of a stochastic point process before and after the stimulus application, whereby the initial reactions are neglected. These should be classified by other methods and notions.

Animals↗
PubMed1984

Cloning and mapping of Saccharomyces cerevisiae photoreactivation gene PHR1.

The yeast Saccharomyces cerevisiae, like most organisms, is able to directly repair pyrimidine dimers by using a photoreactivating enzyme and visible light. Cells carrying the phr1 mutation were shown previously to be unable to photoreactivate dimers, but neither the map position nor the primary gene product of the PHR1 gene has been determined. We have cloned this gene and determined its map position. A plasmid containing a 6.4-kilobase yeast DNA insert has been isolated and shown to restore photoreactivation in a phr1 strain. A 3.1-kilobase subclone has also been shown to complement phr1. The original plasmid was targeted to integrate into chromosomal DNA at a site homologous to the insert by cutting within the insert. Two of these integrants have been mapped on the right arm of chromosome XV; the integrants have been further mapped at ca. 13 centimorgans from prt1. It has also been independently determined that phr1 maps at this location. Thus, we have determined the map position of PHR1 and also have shown that the plasmid contains PHR1 rather than a suppressor of the phr1 mutation.

Chromosome Mapping↗
PubMed1984

Coordination of neuronal signals as structures in state space.

This paper expresses difficulties we have in interpreting neuronal activities by means of information and probability theory: until now there is no general agreement about the alphabet used by the neurons and, consequently, the first step in information theory is actually a conjecture. Further, electrophysiological single unit records can often be shown to be not stationary (because of trends, facilitations, inhibitions, transient reactions or oscillations). Thus they would not appear to be ergodic. But then, how does the system succeed in recognizing certain patterns by only one realization of a stochastic process? These difficulties do not arise if an appropriate multiunit system is considered, the dynamics of which are determined by a set of differential equations. The asymptotic (t----infinity) solutions of these equations define a number of state space structures (fixed points, limit cycles or strange attractors). According to this concept, information is related to the special shape of a state space structure and its probability, and information flow means the filtering of these structures.

Animals↗
PubMed1983

A note on the use of serial measures in spike train analysis and their relation to the corresponding moments.

A spike train is a sequence of interspike intervals and should be described in terms of random variables. So, in order to recognize the information of the spike train, one usually calculates the sample mean (as the normalized sum of all intervals in one realization) or the means (of outcomes of respective intervals), an approximation of which is the PSTH. Further, the sample variance and variance, the serial correlation, and the autocovariance are utilized for evaluation. In this paper it is shown that these notions, which seem to be very similar, have little to do one with another, except for some cases (stationarity, ergodicity), which rarely occur in neurobiology. Finally, it is proposed to rename the term stationarity in spike train analysis, because it differs considerably from the definition which is used in the theory of random variables and stochastic processes.

Action Potentials↗
PubMed1982

An efficient method for the Fourier transform of a neuronal spike train.

A spike train may be represented by a superposition of Dirac delta-functions. One of the simplest ways of converting such a comb function into a continuous function is to use a Fourier transform. In general there are two possibilities, both of which have their disadvantages: the direct transform which is extremely time-consuming, and the fast Fourier transform of the low pass filtered comb function; the latter method, although quicker, often requires a greater storage capacity than is readily available. In the present paper, therefore, a third possibility is suggested. Essentially, it is a direct Fourier transform which takes advantage of certain properties of a spike train. The corresponding algorithm works much faster than a common Fourier transform.

Animals↗
PubMed1981

Mitotic chromosome loss in a radiation-sensitive strain of the yeast Saccharomyces cerevisiae.

Cells of Saccharomyces cerevisiae with mutations in the RAD52 gene have previously been shown to be defective in meiotic and mitotic recombination, in sporulation, and in repair of radiation-induced damage to DNA. In this study we show that diploid cells homozygous for rad52 lose chromosomes at high frequencies and that these frequencies of loss can be increased dramatically by exposure of these cells to x-rays. Genetic analyses of survivors of x-ray treatment demonstrate that chromosome loss events result in the conversion of diploid cells to cells with near-haploid chromosome numbers.

Chromosome Aberrations↗
PubMed1980

Diploid spore formation and other meiotic effects of two cell-division-cycle mutations of Saccharomyces cerevisiae.

The meiotic effects of two cell-division-cycle mutations of Saccharomyces cerevisiae (cdc5 and cdc14) have been examined. These mutations were isolated by L.H. HARTWELL and his colleagues and characterized as defective in mitosis, causing a temperature-sensitive arrest in late nuclear division. When subjected to the restrictive temperature in meiosis, diploid cells homozygous for either of these mutations generally proceeded through premeiotic DNA synthesis and commitment to meiotic levels of recombination, but then arrested at a stage following spindle pole body (SPB) duplication and separation. The two SPBs lacked the interconnection by spindle microtubules typical of the complete meiosis I spindle. Challenge of these homozygotes by a semi-restrictive temperature often caused the production of asci containing two diploid spores. Genetic analysis of the viable pairs of spores revealed that each spore had become homozygous for centromere-linked markers significantly more frequently than for distal markers, indicating that the two spores each contained pairs of sister centromeres that had co-segregated in the reductional division of meiosis I. Ultrastructural analysis of the cdc5 homozygote demonstrated that these cells had completed meiosis I and formed two meiosis II spindles, but that the latter remained unusually short. This resulted in the encapsulation of both poles of each spindle within a single spore wall. These mutations therefore are defective in both meiotic divisions, as well as in the mitotic division described originally.

Cell Cycle↗
PubMed1978

Meiotic effects of DNA-defective cell division cycle mutations of Saccharomyces cerevisiae.

The meiotic effects of several cell division cycle (cdc) mutations of Saccharomyces cerevisiae have been investigated by electron microscopy and by genetic and biochemical methods. Diploid strains homozygous for cdc mutations known to confer defects on vegetative DNA synthesis were subjected to restrictive conditions during meiosis. Electron microscopy revealed that all four mutants were conditionally arrested in meiosis after duplication of the spindle pole bodies but before spindle formation for the first meiotic division. None of these mutants became committed to a recombination or contained synaptonemal complex at the meiotic arrest.--The mutants differed in their ability to undergo premeiotic DNA synthesis under restrictive conditions. Both cdc8 and cdc21, which are defective in the propagation of vegetative DNA synthesis, also failed to undergo premeiotic DNA synthesis. The arrest of these mutants at the stage before meiosis I spindle formation could be attributed to the failure of DNA synthesis because inhibition of synthesis by hydroxyurea also caused arrest at this stage.--Premeiotic DNA synthesis occurred before the arrest of cdc7, which is defective in the initiation of vegetative DNA synthesis, and of cdc2, which synthesizes vegetative DNA but does so defectively. The meiotic arrest of cdc7 homozygotes was partially reversible. Even if further semiconservative DNA replication was inhibited by the addition of hydroxyurea, released cells rapidly underwent commitment to recombination and formation of synaptonemal complexes. The cdc7 homozygote is therefore reversibly arrested in meiosis after DNA replication, whereas vegetative cultures have previously been shown to be defective only in the initation of DNA synthesis.

Cell Cycle↗
PubMedDate not supplied

The contribution of homologous recombination in preserving genome integrity in mammalian cells.

Although it is clear that mammalian somatic cells possess the enzymatic machinery to perform homologous recombination of DNA molecules, the importance of this process in mitigating DNA damage has been uncertain. An initial genetic framework for studying homologous recombinational repair (HRR) has come from identifying relevant genes by homology or by their ability to correct mutants whose phenotypes are suggestive of recombinational defects. While yeast has been an invaluable guide, higher eukaryotes diverge in the details and complexity of HRR. For eliminating DSBs, HRR and end-joining pathways share the burden, with HRR contributing critically during S and G2 phases. It is likely that the removal of interstrand cross-links is absolutely dependent on efficient HRR, as suggested by the extraordinary sensitivity of the ercc1, xpf/ercc4, xrcc2, and xrcc3 mutants to cross-linking chemicals. Similarly, chromosome stability in untreated cells requires intact HRR, which may eliminate DSBs arising during DNA replication and thereby prevent chromosome aberrations. Complex regulation of HRR by cell cycle checkpoint and surveillance functions is suggested not only by direct interactions between human Rad51 and p53, c-Abl, and BRCA2, but also by very high recombination rates in p53-deficient cells.

Amino Acid Sequence↗
PubMedDate not supplied

An endomitotic effect of a cell cycle mutation of Saccharomyces cerevisiae.

A recessive temperature-sensitive mutation of Saccharomyces cerevisiae has been isolated and shown to cause an increase in ploidy in both haploids and diploids. Genetic analysis revealed that the strain carrying the mutation was an aa diploid, although MNNG mutagenesis had been done on an a haploid strain. When the mutant strain was crossed with an alpha alpha diploid and the resultant tetraploid sporulated, some of the meiotic progeny of this tetraploid were themselves tetraploid, as shown by both genetic analysis and DNA measurements, instead of diploid as expected of tetraploid meiosis. The ability of these tetraploids to continue to produce tetraploid meiotic progeny was followed for four generations. Homothallism was excluded as a cause of the increase in ploidy; visual pedigree analysis of spore clones to about the 32-cell stage failed to reveal any zygotes, and haploids that diploidized retained their mating type. An extra round of meiotic DNA synthesis was also considered and excluded. It was found that tetraploidization was independent of sporulation temperature, but was dependent on the temperature of germination and the growth of the spores. Increase in ploidy occurred when the spores were germinated and grown at 30 degrees, but did not occur at 23 degrees. Two cycles of sporulation and growth at 23 degrees resulted in haploids, which were shown to diploidize within 24 hr when grown at 30 degrees. Visual observation of the haploid cells incubated at 36 degrees revealed a cell-division-cycle phenotype characteristic of mutations that affect nuclear division; complementation analysis demonstrated that the mutation, cdc31-2, is allelic to cdc31-1, a mutation isolated by Hartwell et al. (1973) and characterized as causing a temperature-sensitive arrest during late nuclear division. The segregation of cdc31-2 in heterozygous diploids was 2:2 and characteristic of a noncentromere-linked gene.

Cell Cycle↗