RESUMO
In humans, ventricular folds are located superiorly to the vocal folds. Under special circumstances such as voice pathology or singing, they vibrate together with the vocal folds to contribute to the production of voice. In the present study, experimental data measured from physical models of the vocal and ventricular folds were analyzed in the light of nonlinear dynamics. The physical models provide a useful experimental framework to study the biomechanics of human vocalizations. Of particular interest in this experiment are co-oscillations of the vocal and ventricular folds, occasionally accompanied by irregular dynamics. We show that such a system can be regarded as two coupled oscillators, which give rise to various cooperative behaviors such as synchronized oscillations with a 1:1 or 1:2 frequency ratio and desynchronized oscillations with torus or chaos. The insight gained from the view of nonlinear dynamics should be of significant use for the diagnosis of voice pathologies, such as ventricular fold dysphonia.
Assuntos
Prega Vocal , Voz , Humanos , Dinâmica não Linear , Fenômenos BiomecânicosRESUMO
A method is proposed to detect the dynamical instability of complex time series. We focus on how the partitioned entropy of an initially localized region of the attractor evolves in time and show that its growth rate corresponds to the first Lyapunov exponent. To avoid spurious detection of the dynamical instability, a criterion is further introduced to distinguish chaos from limit cycles or tori. Numerical experiments using prototypical models of chaotic systems demonstrate that the growth rate of the partitioned entropy indeed provides a good estimate of the first Lyapunov exponent. The method is also shown to be robust against observational noise and dynamical noise. Analysis of experimental data measured from a physical model of the vocal folds highlights the practical applicability of the present method to real-world data. Advantages of the present method over conventional methods are also discussed.
RESUMO
Late-onset hypogonadism, a male age-related syndrome characterized by a decline in testosterone production in the testes, is commonly treated with testosterone replacement therapy, which has adverse side effects. Therefore, an alternative treatment is highly sought. Supplementation of a high dosage of biotin, a water-soluble vitamin that functions as a coenzyme for carboxylases involved in carbohydrate, lipid, and amino acid metabolism, has been shown to influence testis functions. However, the involvement of biotin in testis steroidogenesis has not been well clarified. In this study, we examined the effect of biotin on testosterone levels in mice and testis-derived cells. In mice, intraperitoneal treatment with biotin (1.5 mg/kg body weight) enhanced testosterone levels in the serum and testes, without elevating serum levels of pituitary luteinizing hormone. To investigate the mechanism in which biotin increased the testosterone level, mice testis-derived I-10 cells were used. The cells treated with biotin increased testosterone production in a dose- and time-dependent manner. Biotin treatment elevated intracellular cyclic adenosine monophosphate levels via adenylate cyclase activation, followed by the activation of protein kinase A and testosterone production. These results suggest that biotin may have the potential to improve age-related male syndromes associated with declining testosterone production.
Assuntos
Testículo , Testosterona , Camundongos , Masculino , Animais , Biotina/farmacologia , Hormônio Luteinizante/metabolismo , Proteínas Quinases Dependentes de AMP Cíclico/metabolismoRESUMO
Vitamins are a family of micronutrients comprising 13 groups of organic compounds, of which vitamin B1 was identified first, approximately 110 y ago. Deficiency of each vitamin results in specific symptoms, such as neuropathy, dermatitis, diarrhea, dementia, pernicious anemia, scurvy, blindness, rickets, and bleeding. Almost all vitamins can modulate the functions of enzymes and/or other proteins involved in the formation of bone and soft tissues, generation of energy, and regulation of homeostasis via specific vitamin-protein interactions. In addition to the well-known physiological roles of vitamins, novel modes of action of vitamins have been elucidated. These new functions could contribute to extending healthy life expectancy by preventing and curing lifestyle-related diseases. In this mini-review, we introduce the functional properties of three vitamins, vitamin B3 (niacin), biotin, and vitamin K, for the prevention of age-related diseases.
Assuntos
Vitamina A , Vitaminas , Vitamina K , Tiamina , Estilo de VidaRESUMO
Hypogonadism, associated with low levels of testosterone synthesis, has been implicated in several diseases. Recently, the quest for natural alternatives to prevent and treat hypogonadism has gained increasing research interest. To this end, the present study explored the effect of S-allyl cysteine (SAC), a characteristic organosulfur compound in aged-garlic extract, on testosterone production. SAC was administered at 50 mg/kg body weight intraperitoneally into 7-week-old BALB/c male mice in a single-dose experiment. Plasma levels of testosterone and luteinizing hormone (LH) and testis levels of proteins involved in steroidogenesis were measured by enzymatic immunoassay and Western blot, respectively. In addition, mouse testis-derived I-10 cells were also used to investigate the effect of SAC on steroidogenesis. In the animal experiment, SAC significantly elevated testosterone levels in both the plasma and the testis without changing the LH level in plasma and increased phosphorylated protein kinase A (p-PKA) levels. Similar results were also observed in I-10 cells. The findings demonstrating the increasing effect of SAC on p-PKA and mRNA levels of Cyp11a suggest that SAC increases the testosterone level by activating the PKA pathway and could be a potential target for hypogonadism therapeutics.
Assuntos
Cisteína/análogos & derivados , Testículo/efeitos dos fármacos , Testículo/metabolismo , Testosterona/biossíntese , Animais , Linhagem Celular , Proteínas Quinases Dependentes de AMP Cíclico/metabolismo , Cisteína/farmacologia , Ativação Enzimática/efeitos dos fármacos , Alho/química , Células Intersticiais do Testículo/efeitos dos fármacos , Células Intersticiais do Testículo/metabolismo , Hormônio Luteinizante/sangue , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Fosforilação , Testículo/citologia , Testosterona/sangueRESUMO
Existing methods for estimating the largest Lyapunov exponent from a time series rely on the rate of separation of initially nearby trajectories reconstructed from the time series in phase space. According to Ueda, chaotic dynamical behavior is viewed as a manifestation of random transitions between unstable periodic orbits in a chaotic attractor, which are triggered by perturbations due to experimental observation or the roundoff error characteristic of the computing machine, and consequently consists of a sequence of piecewise deterministic processes instead of an entirely deterministic process. Chaotic trajectories might have no physical reality. Here, we propose a mathematical method for estimating a surrogate measure for the largest Lyapunov exponent on the basis of the random diffusion of the symbols generated from a time series in a chaotic attractor, without resorting to initially nearby trajectories. We apply the proposed method to numerical time series generated by chaotic flow models and verify its validity.
RESUMO
It is known that biotin prevents the development of diabetes by increasing the functions of pancreatic beta-cells and improving insulin sensitivity in the periphery. However, its anti-obesity effects such as anorectic effects remain to be clarified. Acetyl CoA carboxylase (ACC), a biotin-dependent enzyme, has two isoforms (ACC1 and ACC2) and serves to catalyze the reaction of acetyl CoA to malonyl CoA. In the hypothalamus, ACC2 increases the production of malonyl CoA, which acts as a satiety signal. In this study, we investigated whether biotin increases the gene expression of ACC2 in the hypothalamus and suppresses food intake in mice administered excessive biotin. Food intake was significantly decreased by biotin, but plasma regulators of appetite, including glucose, ghrelin, and leptin, were not affected. On the other hand, biotin notably accumulated in the hypothalamus and enhanced ACC2 gene expression there, but it did not change the gene expression of ACC1, malonyl CoA decarboxylase (a malonyl CoA-degrading enzyme), and AMP-activated protein kinase α-2 (an ACC-inhibitory enzyme). These findings strongly suggest that biotin potentiates the suppression of appetite by upregulating ACC2 gene expression in the hypothalamus. This effect of biotin may contribute to the prevention of diabetes by biotin treatment.