Biomedical subjects
Publications and source records attributed to G T Matioli.
In general terms the paper discusses the relevance of mitotically quiescent, malignant cells for increasing resistance to chemotherapy. Detailed are some routes to Go for malignancies either dependent or autonomous for their mitotic potential.
The paper discusses malignant transformation of myeloid precursors that had atypical renewal in vivo. Their in vitro transformation rate disproportionates clinical incidences. Besides composition differences of transforming agents, this is due to quali-quantitative deficiencies of multitask growth factors added to empirical cultures. In combination these anomalies perturb the web of differentiation path, whose robustness minimizes clonal transformation in vivo.
On the basis of numerical and kinetic data, the paper argues against the tenet that BCR-Abl is sufficient for transforming into Chronic Myelogenous leukemia a human hemopoietic stem cell, regardless of degree of pluripotency.
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This paper discusses a mechanism for converting heterochromatin into the more relaxed state of euchromatin. Actuation of such state conversion stems from disassembly of internal vesicles that are incapable of surviving when trapped within the inner chamber of mammalian nuclei.
The paper discusses how the environment of regional lymph nodes optimizes growth of metastatic cells shed by non-autonomous tumoral primaries.
Disentanglement of centromeric braids is refined in 3 dimensions. Besides expanding the combinatronics of chromatid polarization in comparison to 2-D formats, the present study discusses certain chromosomal anomalies such as the statistics of isochromatids and variants thereof in cancer cells.
Using order parameters from field theory, the paper rationalizes the statistics of myeloid and erythroid leukemias more satisfactorily than the random mutation hypothesis. Adapted to B- and plasma cell lineages, the same arguments conceptualize the statistics of related malignancies congruently to clinical findings.
The paper proposes a mechanism for regulating nucleo-cytoplasmic exchanges of macromolecules via NPC in vertebrates. Bending of NE toward the transport vector significantly contributes to the dynamics.
We investigate how chromatin entanglements may subvert the topology of DNA segments (and of genes therein) whenever sister chromatids separate by eversion. Such subversions offer interesting ideas on how identical genes may be differently or identically expressed after segregation of sister chromatids.
The paper discusses how a DNA strand contributes pivots that distributively interconnect the jaws of two or more C units of a chromatid stack. Rather than being static, the location of these pivots may be shifted according to alternative modes without compromising the chromatid's physical integrity.
The paper discusses a mechanism for segmental insertions (ins) between two chromatids. In human cancers, such rearrangements are significantly less frequent than reciprocal translocations (rt). Regarding the clinical incidence of ins versus rt, the proposed dynamics is more satisfactory than the random mutation hypothesis.
This paper discusses a mechanism whereby a sister replica unit separates from its template via a flip-rotation rather than by eversion. Such an unusual process engenders a permanent antidromic sequence, as well as two (evanescent) kinks only on the stack of the replicated chromatid.
The paper discusses a mechanism for semiconservative duplication of a pair of centrioles from a single parent. The mechanism accounts for the (transient or permanent) quasi-orthogonality of mammalian centrioles.
The paper studies mammalian chromatids conformed as donut-like rings. Albeit enacting many topologic and dynamic aspects of straight chromatids (e.g. replication, eversion, antipodal segregation at anaphase, etc.), rings differ in certain properties regarding in particular disposal of soliton-like, kinked frustrations of their chirality during recurrent sister chromatid exchanges (SCEs).
The paper discusses a mechanism apt to convert the topology of a straight chromatid into one that could lead to the formation of a O-ring. It is predicted that such conversions might occur only in exceptional circumstances, due to a combination of poorly correlated events.
After considering few alternative possibilities, it is concluded that eversion is the most efficient mechanism for disengagement of replica chromatids from their templates.
The paper discusses a mechanism for short-long duplications of segments of somatic chromatids in cancer cells. Based on the Frenkel-Kontorova model, the mechanism accounts for the high incidence of duplications on the long arm of almost all chromatids.