14 research outputs found

    Applications of Human Tissue-Engineered Blood Vessel Models to Study the Effects of Shed Membrane Microparticles from T-Lymphocytes on Vascular Function

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    Microparticles (MPs) are membrane vesicles harboring cell surface proteins and containing cytoplasmic components of the original cell. High levels of circulating MPs have been detected in pathological states associated with vascular dysfunction. We took advantage of the self-assembly method of tissue engineering to produce in vitro three vascular constructs from human vascular smooth muscle cells and fibroblasts to investigate the role of the adventitia in the modulation of vascular tone by MPs, comparing the contractile response of each of these constructs to histamine. The first two were composed of an adventitia (tissue-engineered vascular adventitia (TEVA)) or a media (tissue-engineered vascular media (TEVM)) solely, and the third one contained a media and an adventitia (tissue-engineered vascular media and adventitia (TEVMA)). In the three constructs, the results show that histamine induces contraction insensitive to blockade of inducible nitric oxide (NO) synthase (iNOS) and cyclooxygenase-2 (COX-2) and not affected by MP treatment. MPs decreased NO production and nuclear factor (NF)-ÎșB expression but did not affect superoxide anion (O2−) release in TEVA. MPs enhanced NF-ÎșB expression but did not affect iNOS and COX-2 expression or NO or O2− release in TEVM. In TEVMA, MPs did not enhance NF-ÎșB expression, but COX-2 expression was higher, and O2− release was lower. Thus, MPs affected NO, O2−, NF-ÎșB, and COX-2 in a subtle fashion to maintain the contractile response to histamine. The use of tissue-engineered vascular constructs results in a better understanding of the effect of MPs on human adventitia and media

    On the energy growth of some periodically driven quantum systems with shrinking gaps in the spectrum

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    We consider quantum Hamiltonians of the form H(t)=H+V(t) where the spectrum of H is semibounded and discrete, and the eigenvalues behave as E_n~n^\alpha, with 0<\alpha<1. In particular, the gaps between successive eigenvalues decay as n^{\alpha-1}. V(t) is supposed to be periodic, bounded, continuously differentiable in the strong sense and such that the matrix entries with respect to the spectral decomposition of H obey the estimate |V(t)_{m,n}|0, p>=1 and \gamma=(1-\alpha)/2. We show that the energy diffusion exponent can be arbitrarily small provided p is sufficiently large and \epsilon is small enough. More precisely, for any initial condition \Psi\in Dom(H^{1/2}), the diffusion of energy is bounded from above as _\Psi(t)=O(t^\sigma) where \sigma=\alpha/(2\ceil{p-1}\gamma-1/2). As an application we consider the Hamiltonian H(t)=|p|^\alpha+\epsilon*v(\theta,t) on L^2(S^1,d\theta) which was discussed earlier in the literature by Howland

    Violence in Mental Disorders and Community Sample: an evolutionary model related with dominance in social relationships

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    The major risk determinants of violence are to be young and male, to have low socioeconomic status and suffering substance abuse. This is true whether it occurs in the context of a concurrent mental illness or not; i.e., mental disorders are neither necessary, nor sufficient causes for violence. Intense motivation is a facilitating factor for violence in clinical and non clinical samples. This explains why ‘normal’ people, are implicated in planned violence at higher rates than mentally ill (e.g. in criminal acts against property). However mentally ill patients are more easily implicated in impulsive violence or in violence without obvious cause due to veiled motivation fuelled by unidentified symptoms. Subjective or real awareness of competitive disadvantage increases motivation for violence (e.g. paranoid, narcissistic symptoms, etc.). Many psychiatric disorders as antisocial disorder, borderline, schizophrenia, have most of the factors that facilitate the appearance of violence. Antisocial disorder is a good model to study determinants of violence in normal samples as it is present in young males that do not have any psychotic symptom, have stable symptomatology, self control under scrutiny, and their motivations are similar to normal samples. Our evolutionary model suggests that there is a non random association of genetic factors (genes, pseudogenes, promoting areas, etc.), that is, a genetic cluster (cluster DO), whose phylogenetic function is to motivate to be the dominant in social relationships. To be the dominant is a major psychological feature present in many social groups of animals, included primates. DO cluster have sense from an evolutionary viewpoint: when expressed in no pathological way it increases inclusive fitness (transmission of the genes of a person genotype whether by oneself or by relatives reproduction). Features of cluster DO in humans are expressed differently according to sex, age, moral education, level of intelligence, etc. Cluster DO has higher phenotypical expression in males and young people. Primary antisocial personality disorder and other related disorders (cluster B personality disorders, disocial, defiant disorder, etc.), are a pathological manifestation of this cluster DO. Some other genetic clusters that causes the genetic liability to some disorders (e.g. attention deficit disorder) are non random associated with cluster DO, thus explaining clinical comorbidity. According to our model, motivation for dominance usually prevails over motivation for material benefit or antinormative behaviour, this explains some incongruent behaviour in antisocial patients not elucidated by other models. Along with the primary expressed feature of dominance of cluster DO there are other secondary features that have been identified by psychobiological studies: novelty seeking, intolerance for frustration, impulsiveness, fearless, aggressiveness, higher threshold for activation of the sympathetic system, lack of empathy, egoism, non acceptance of rules, defiant and rebellious behaviour, manipulation in social interactions, selfishness and deficits in altruism or in social co-operation
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