Biomedical subjects
Publications and source records attributed to G T Matioli.
The paper discusses the dynamics of reciprocal translocations between chromatids in general terms. The mechanism accounts for the high frequency of these anomalies in cancer cells with nuclei distorted by permanent or transient deformations of their envelopes.
The paper discusses modulation of telomere length by mechanisms that do not require telomerase. Although ultimately dependent upon the cell's mitotic potential, these mechanisms do not sufficiently discriminate between normal and malignant cells.
A mechanism for converting human chromatid 17 into its isoforms-isochromatid 17q and isochromosome X17q--is discussed. The frequency of these isoforms in a subset of Ph+ chronic myeloid leukemia patients is traceable to singularities of the nuclear envelope of myeloid cells. When statistically interpreted, loss of tumor suppressor gene (p53) seems less significant than additive retention of genes on the q arm of 17, at least regarding evolution of clones carrying both Ph and X17q markers.
Rescaling of chromatid C units into similar but smaller epsilon (epsilon) subunits is discussed. When subverted, these subunits are responsible for repositioning genes in different states of transcriptional accessibility via an analogy in miniature of more massive sister chromatid exchanges.
The paper discusses a mechanism for reciprocal translocation of midsegments between two chromatids so that one of the segments is restacked in inverted configuration. Regarding malignant cells, such process could derive from anachronistic assembly of the nuclear envelope.
Logical scrutiny of the axiom of randomness argues against its reliability as an objective criterion for interpreting the insurgence of mutations in cancer cells. We propose that chaos theory is preferable because it is conceptually much more robust.
The paper discusses a mechanism whereby symmetry group actions synergised by a nuclear vesicle and a kink yield either single or double inversions and/or other misorientations of relatively short DNA sequences and genes on small chromatid sections.
Concepts from Lagrangian variationals are adapted to rationalize both statistics and evolution of certain non-holonomic gene rearrangements in certain leukemias (such as chronic myeloid leukemia) as well as in a significant proportion of healthy individuals.
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The paper studies how the Apollonian dynamics of clustered chromatids contributes to optimize pairing between homologs in mitosing mammalian spermatogonia, particularly so during anaphase.
The paper discusses a type of transcriptional entrainment between master-slave genes that is occasioned by the translation of a solitonic kink along the stack of a coiled chromatid.
The paper studies how certain topologic features of the nuclear envelope may reorganize entrained transcription via spatial rearrangements of genes carried by distinct chromatids.
The centriole is conjectured as functioning as an 'autopilot', able to correct spindle orientation and polarity in highly deformed cells.
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The paper discusses certain distributive and clustering modes of stimulus P and of its receptors. When combined with topologic features peculiar to sources and stem cells, these parameters account not only for the cycling variations typical of normal stem cells but also for seemingly paradoxical shifts in proliferative activity of cells grafted into patients with chronic myeloid leukemias.
The paper discusses certain dynamic processes leading to meiotic (haploid) partition of chromatids via the chiasmatic mode in mammalian spermatic cells. The achiasmatic case is also reviewed briefly and only in the context of homologs with centromeric braids arrayed in the Para configuration.
This note comments on a mechanism for pairing homologous chromatids. Of interest are two modes: Ortho and Para. Although both yielding antihelical duplexes, the two modes are not equivalent regarding cladistic relations between homologs.
This note complements a previous one (1), regarding in particular, mitotic separation of replica homologs from their templates, in mammalian spermatogonia. Topological differences between Ortho- and Para-braids determine different modes of antipodal segregation of paired homologs prior to onset of meiosis.