Thesis (doctoral)--University of Tartu, 2006. / This dissertation is based on 3 papers. Includes bibliographical references.

In this thesis, we investigate the contraction reconstruction conjecture. It states that all simple graphs with at least four edges are reconstructible, that is they are uniquely determined from their collection of single edge contraction minors, called the deck. Similar questions have been studied in the past, the vertex reconstruction conjecture being the most famous. There are usually two steps to show that a class of graph is reconstructible. The first one is to show that the class is recognizable, meaning that it is possible to determine if a graph G belongs to that class by looking at its deck. In order to recognize some classes of graphs, we show that a wide range of graph properties are reconstructible. We investigate the connectivity of graphs, which is useful to recognize disconnected, separable, and 2-connected graphs. We also show that the number of cycles of various lengths, the degree sequence, the number of spanning trees, the planarity, the presence of cliques of various sizes, and the diameter are reconstructible. Knowing the lengths of cycles allows us to recognize the class of bipartite graphs, while knowing the degree sequence allows us to recognize regular graphs. The second step in showing that a class of graph is reconstructible is called weak reconstruction. We say that a class of graph is weakly reconstructible if no two graphs in that class share the same deck. A class of graphs that is both weakly reconstructible and recognizable is reconstructible. In this thesis, we show that disconnected graphs, bipartite graphs, most separable graphs and most 2-edge connected graphs are reconstructible. We also show that distance regular graphs and some cubic graphs are reconstructible. We quickly delve into the theory of probabilities to give a proof that almost all graphs are reconstructible. Finally, the relation between edge contraction and graph automorphisms is studied. We study the automorphism group of a graph in relation to those of its cards. We also study the concept of contraction pseudo-similarity. Two edges are contraction pseudo-similar if they are not similar, but their contractions yield isomorphic graphs. We completely characterize the graphs that contain contraction pseudo-similar edges.

Understanding the physiology of pregnancy enables effective management of pregnancy complications that could otherwise be life threatening for both mother and fetus. A functional uterus (a) retains the fetus in utero during pregnancy without initiating stretch-induced contractions and (b) is able to dilate the cervix and contract the myometrium at term to deliver the fetus. The onset of labour is associated with successful cervical remodelling and contraction of myometrium, arising from concomitant activation of uterine immune and endocrine systems. A large body of evidence suggest that the action of local sex hormones may drive changes occurring in the uterine microenvironment at term. Although there have been a number of studies considering the potential role(s) played by progesterone and estrogens at the time of parturition, the role of androgens has received less scrutiny. The overarching aim of this thesis was to investigate the potential roles of androgens in myometrial biology at the time of pregnancy. We examined both the genetranscription dependent (genomic) and independent (non-genomic) action of androgens on the uterine smooth muscle, employing in vitro, ex vivo, and in vivo approaches. We found that the androgen receptor (AR) mRNA was significantly increased in the myometrium during labour when compared to the term non-labouring myometrium. Our gene expression studies revealed that ligand-dependent AR signalling in the myometrium might play a role in regulation of uterine smooth muscle cell contractility. We explored the effect of androgens on contraction of uterine smooth muscle strips obtained from both human myometrial biopsies collected at term and murine uterine horns. We found that testosterone (T) and dihydrotestosterone (DHT) in a range of 10-100 μM concentrations rapidly relaxed spontaneous and oxytocin-initiated contractions. The relaxant effect was not mediated by the classical intracellular AR nor was cell-surface initiated as shown by experiments employing a specific AR antagonist (flutamide) and a cell-surface impermeable androgen (TBSA). We investigated whether the relaxant effect was specific to androgens or a generic effect of sex hormones. We demonstrated that both estradiol (E2) and progesterone (P4) were also capable of relaxing the human and murine myometrium at the same dose range. In addition, a sex hormone “cocktail” (all four sex hormones combined at 10 μM dose each) mimicked the relaxant effect that each individual sex hormone elicited at a 40 μM dose, implying that the effect was possibly attributable to the steroid structure of the sex hormones. To study the underlying molecular events that mediate the relaxant effect of sex hormones observed ex vivo, we employed two human myometrial cell lines namely PHM1-41s and UtSMCs. We demonstrated that the androgen-induced relaxation in vitro was not induced by cell death but was mediated by a physiological mechanism whereby incubation with the androgen impaired the stimulated-Ca2+ entry into the uterine myocytes, which in turn resulted in poor phosphorylation of myosin light chain protein. Finally, we conducted a pilot study to explore the hypothesis that administration of androgen could relax the uterine muscle in vivo. We utilised a mouse model of infection-induced preterm labour, where infection was induced by intrauterine administration of liposaccharide (LPS) on day 17 of murine pregnancy. Our preliminary data showed that intrauterine administration of DHT on day 17 did not significantly reduce the rate of LPS-induced preterm birth in the doses tested in this study. In conclusion, the androgen-induced in vitro tocolysis appears to be sex hormone-specific rather than androgen-specific. Therefore, sex hormones might have the potential to be used for effective in vivo tocolysis to inhibit premature-initiated contractions. Our investigation of the androgen-dependent signalling in the myometrium contributed to the development of novel hypotheses regarding the role of androgens in the regulation of the phenotypic transition of MSMCs during pregnancy. These hypotheses remain to be confirmed in future studies.

Standard local control theory, which describes Ca²⁺ release during excitation-contraction coupling (ECC), assumes that all Ryanodine Receptor (RyR) complexes are equivalent. Recent data from our laboratory has called this assumption into question. Specifically, we have shown that RyR complexes in ventricular myocytes differ depending on their location within the cell. This, and other data, has led us to hypothesize that similar differences occur within the rat atrial cell. To test this hypothesis, we have triple-labeled enzymatically-isolated, fixed myocytes to examine the distribution and colocalization of RyR, calsequestrin (CSQ), voltage-gated Ca²⁺ channels (Cav1.2), sodium-calcium exchangers (NCX), and caveolin-3 (cav-3). All images were acquired on a wide-field microscope, deconvolved, and subject to extensive analysis, including a novel method of measuring statistical significance of the recorded colocalization values. Overall, eight surface RyR populations were identified, depending on its binding partners. One of these groups, in which RyR, Cav1.2, and NCX colocalize, may provide the structural basis for ‘eager’ sites of Ca²⁺ release in atria, while other groups were defined based on their association with cav-3, and are therefore highly likely to be under the influence of other signaling molecules located within caveolae. Importantly, although a small portion of the surface RyR in atria do colocalize with NCX alone, the majority are tightly linked to Cav1.2 alone or Cav1.2 and NCX together. Therefore, it appears likely that Cav1.2-mediated calcium-induced calcium release (CICR) is the primary method of initiating Ca²⁺ release from the SR during EC coupling. / Medicine, Faculty of / Cellular and Physiological Sciences, Department of / Graduate

No description available.

Eight men and 8 women trained 3 days/ week for 16 weeks by doing attempted ballistic unilateral ankle dorsiflexions against resistance which either rendered the resultant contraction isometric (one limb) or allowed a relatively high velocity (joint angular velocity of 5.23 rad.s- 1 ) isokinetic concentric contraction (other limb). Training sessions consisted of 5 sets of 10 contractions of each type. Pre and post-training tests of peak torque at 0, 0.26, 0.52, 1.04, 1.55, 3.02, 4.19, 5.23 rad.s-1 indicated a velocity specific training response (p<0.01), with increases of -5.9, 5.6, 8.6, 15.3, 13.9, 14.1, 19.3, and 27.4% respectively. In a separate test, maximal voluntary isometric peak torque (6 .1%) and maximum rates of torque development (20.4%) and relaxation (31.5%) increased after training (p<0.01). Electrically evoked isometric tetanic peak torque and rate of torque relaxation did not change but rate of torque development increased 12. 6% ( p<0. 01). Evoked peak twitch torque did not change but time to peak torque and 1/2 relaxation time decreased 6.2 and 11.9% respectively (p<0.01). Electromyographic (EMG) recordings of the agonist tibialis anterior (TA) during test contractions showed no change in integrated EMG, but there was an increase (14.6%, p<0.05) in antagonist soleus (S) EMG from mid-test to post-test. The velocity specific response to the isometric and isokinetic concentric training modes was the same, indicating that it was the intent to make a ballistic contraction, rather than the resultant velocity of contraction, that determined the velocity specific response. The data also suggest that both neural and muscular adaptations contributed to the velocity specific training response / Thesis / Master of Science (MS)

Extraction and quantitation of myosin light chain two coupled with myograph recordings from Ascaris muscle perfused with calmodulin inhibitors and neurotransmitters in conjunction with their respective agonists and antagonists have been used to establish the regulation of contraction in this muscle. Densitometric tracings of isolectric focusing gels separating the regulatory light chain were used to quantitate phosphorylation in resting, contracted and flaccid muscle. These studies indicated that inhibitory neurostimulation is mediated by a true GABA receptor. Myosin-mediated contraction is responsible for maintaining the level of tension observed in resting actin-mediated muscle. Actin-mediated contraction is responsible for the rapid rise in tension following excitatory stimuli. Both systems function simultaneously and are independant.

No description available.

Autogenous shrinkage is of concern in high performance concrete mixtures, when specific properties like strength and durability are enhanced. Factors like low watercement ratio, low porosity and increased hydration kinetics which are associated with high performance concrete mixtures are also responsible for the development of autogenous shrinkage. With about two decades of research into autogenous shrinkage, uncertainties still exist with testing procedure, effect of supplementary cementitious materials, modelling and prediction of autogenous shrinkage. The primary focus of this study is to understand mechanisms which have been postulated to cause autogenous shrinkage like chemical shrinkage and self desiccation. In addition, this study has considered properties like porosity and internal empty voids in the analysis of the causes of bulk volume deformations of the cementitious paste systems with and without mineral admixtures. The study begins with an experimental investigation of chemical shrinkage in hydrating cementitious paste systems with the addition of fly ash, slag and silica fume using the test method recently accepted by the ASTM. This was followed by the experimental investigation of autogenous shrinkage in cementitious paste. The autogenous shrinkage in paste mixtures is studied from an early age (~1.5 hours after addition of water) for cementitious systems at a water-cementitious ratio of 0.32 (w/c 0.25 for limited mixture proportions). A non-contact measurement method using eddy current sensors were adopted. The hydration mechanism of the cementitious paste systems was then modelled using CEMHYD3D, which is a 3 dimensional numerical modelling method successfully used to study, simulate and present the hydration developments in cementitious systems. Properties like chemical shrinkage, degree of hydration, total porosity and free water content; all of which have been obtained from the CEMHYD3D simulation have been cross correlated with the experimental results in order to more comprehensively understand the mechanism contributing to bulk volume change under sealed conditions. The experimental investigations are extended to study the development in concrete with and without mineral admixtures (i.e., silica fume, fly ash and slag). Self desiccation driving the development of autogenous shrinkage has been used extensively across literature but as an alternative the author has proposed using internal drying factor in modelling autogenous shrinkage. The "internal drying factor" is described as the ratio of the empty voids (due to chemical shrinkage) to the total porosity at any point of time of hydration. Independent of the mixture proportions, a linear trend was observed between the autogenous shrinkage strain and increase in internal drying factor. Thus the internal drying factor could be incorporated into semiempirical models while attempting to predict autogenous shrinkage. An increase in the compressive strength of matured concrete at 1 year had a strong correlation to the observed autogenous shrinkage strains irrespective of the cementitious system. It is believed this could be because of the increase in gel-space ratio which is intern linked to the degree of hydration and porosity of the microstructure. The author has obtained strong evidence that the micro-structural changes associated with high strength and durable concrete have a direct impact on the autogenous shrinkage of concrete. Hence, the author suggests that autogenous shrinkage should be investigated and allowable values be stipulated as design criterion in structures that use high strength-high performance concrete.

A pair of commuting bounded operators (S, P) for which the set r = {(z 1 +z 2,z 1z 2) : |z 1| ≤1, |z 2| ≤1} C2 is a spectral set, is called a r-contraction in the literature. For a contraction P and a bounded commutant S of P, we seek a solution of the operator equation S –S*P = (I –P*P)½ X(I –P*P)½ where X is a bounded operator on Ran(I – P*P)½ with numerical radius of X being not greater than 1. We show the existence and uniqueness of solution to the operator equation above when (S,P) is a r-contraction. We call the unique solution, the fundamental operator of the r-contraction (S,P). As the title indicates, there are three parts of this thesis and the main role in all three parts is played by the fundamental operator. The existence of the fundamental operator allows us to explicitly construct a r-isometric dilation of a r-contraction (S,P), whereas its uniqueness guarantees the uniqueness of the minimal r-isometric dilation. The fundamental operator helps us to produce a genuine functional model for pure r-contractions. Also it leads us to a complete unitary invariant for pure r-contractions. We decipher the structures of r-isometries and r-unitaries by characterizing them in several different ways. We establish the fact that for every pure r-contraction (S,P), there is a bounded operator C with numerical radius being not greater than 1 such that S = C + C* P. When (S,P) is a r-isometry, S has the same form where P is an isometry commuting with C and C*. Also when (S,P) is a r-unitary, S has the same form too with P and C being commuting unitaries. Examples of r-contractions on reproducing kernel Hilbert spaces and their dilations are discussed.