Cough is one of the most important defensive reflexes. However,
extensive non- productive cough is a harmful mechanism leading
to the damage of human airways. Cough is initiated by activation
of vagal afferents in the airways. The site of their convergence is
particularly the nucleus of the solitary tract (nTS). The secondorder neurons terminate in the pons, medulla and spinal cord and
there is also the cortical and subcortical control of coughing. Upper
airway cough syndrome (UACS) – previously postnasal drip
syndrome - is one of the most common causes of chronic cough
together with asthma and gastroesophageal reflux. The main
mechanisms leading to cough in patients with nasal and sinus
diseases are postnasal drip, direct irritation of nasal mucosa,
inflammation in the lower airways, upper airway inflammation and
the cough reflex sensitization. The cough demonstrated by UACS
patients is probably due to hypersensitivity of the upper airways
sensory nerve or lower airways sensory nerve, or a combination of
both. Further studies are needed to clarify this mechanism.
Obstructive sleep apnoea syndrome (OSAS) is a common disorder associated with upper airway muscle dysfunction. Agents that improve respiratory muscle performance may have considerable therapeutic value. We examined the effects of acute exposure to sustained and intermittent hypoxia on rat pharyngeal dilator muscle function. Additionally, we sought to test the efficacy of antioxidant treatment in ameliorating or preventing hypoxia-related muscle dysfunction. Isometric contractile and endurance properties of isolated rat sternohyoid muscle bundles were examined at 35 °C in vitro. Muscle bundles were exposed to one of four gas treatments: hyperoxia (control), sustained hypoxia (SH), intermittent hypoxia (IH) or hypoxia/reoxygenation (HR), in the absence or presence of the superoxide scavenger – Tempol (10 mM). Stress-frequency relationship was determined in response to electrical stimulation (10-100 Hz in increments of 10-20 Hz, train duration: 300 ms). Muscle performance was also assessed during repetitive muscle stimulation (40 Hz, 300 ms every 2 s for 2.5 min). Compared to control, IH and HR treatments significantly decreased sternohyoid muscle force. The negative inotropic effect of the two gas protocols was similar, but both were of lesser magnitude than the effects of SH. SH, but not IH and HR, increased muscle fatigue. Tempol significantly increased sensitivity to stimulation in all muscle preparations and caused a leftward shift in the stressfrequency relationship of IH and SH treated muscles. Tempol did not ameliorate sternohyoid muscle fatigue during SH. We conclude that Tempol increases upper airway muscle sensitivity to stimulation but only modestly ameliorates respiratory muscle weakness during intermittent and sustained hypoxic conditions in vitro. Respiratory muscle fatigue during sustained hypoxia appears unrelated to oxidative stress., J. R. Skelly, ... [et al.]., and Obsahuje seznam literatury
In this paper, we develop computational procedures to approximate the spectral abscissa of the switched linear system via square coordinate transformations. First, we design iterative algorithms to obtain a sequence of the least μ1 measure. Second, it is shown that this sequence is convergent and its limit can be used to estimate the spectral abscissa. Moreover, the stopping condition of Algorithm 1 is also presented. Finally, an example is carried out to illustrate the effectiveness of the proposed method.
We present a lower and an upper bound for the second smallest eigenvalue of Laplacian matrices in terms of the averaged minimal cut of weighted graphs. This is used to obtain an upper bound for the real parts of the non-maximal eigenvalues of irreducible nonnegative matrices. The result can be applied to Markov chains.
For a graph property $\mathcal {P}$ and a graph $G$, we define the domination subdivision number with respect to the property $\mathcal {P}$ to be the minimum number of edges that must be subdivided (where each edge in $G$ can be subdivided at most once) in order to change the domination number with respect to the property $\mathcal {P}$. In this paper we obtain upper bounds in terms of maximum degree and orientable/non-orientable genus for the domination subdivision number with respect to an induced-hereditary property, total domination subdivision number, bondage number with respect to an induced-hereditary property, and Roman bondage number of a graph on topological surfaces.
It is one of the fundamental and challenging problems to determine the node numbers of hidden layers in neural networks. Various efforts have been made to study the relations between the approximation ability and the number of hidden nodes of some specific neural networks, such as single-hidden-layer and two-hiddenlayer feedforward neural networks with specific or conditional activation functions. However, for arbitrary feedforward neural networks, there are few theoretical results on such issues. This paper gives an upper bound on the node number of each hidden layer for the most general feedforward neural networks called multilayer perceptrons (MLP), from an algebraic point of view. First, we put forward the method of expansion linear spaces to investigate the algebraic structure and properties of the outputs of MLPs. Then it is proved that given k distinct training samples, for any MLP with k nodes in each hidden layer, if a certain optimization problem has solutions, the approximation error keeps invariant with adding nodes to hidden layers. Furthermore, it is shown that for any MLP whose activation function for the output layer is bounded on R, at most k hidden nodes in each hidden layer are needed to learn k training samples.
The paper deals with the existence of a quasi continuous selection of a multifunction for which upper inverse image of any open set with compact complement contains a set of the form $(G\setminus I)\cup J$, where $G$ is open and $I$, $J$ are from a given ideal. The methods are based on the properties of a minimal multifunction which is generated by a cluster process with respect to a system of subsets of the form $(G\setminus I)\cup J$.
Let $R$ be an integral domain with quotient field $K$ and $f(x)$ a polynomial of positive degree in $K[x]$. In this paper we develop a method for studying almost principal uppers to zero ideals. More precisely, we prove that uppers to zero divisorial ideals of the form $I = f(x)K[x] \cap R[x]$ are almost principal in the following two cases: – $J$, the ideal generated by the leading coefficients of $I$, satisfies $J^{-1} = R$. – $I^{-1}$ as the $R[x]$-submodule of $K(x)$ is of finite type. Furthermore we prove that for $I = f(x)K[x] \cap R[x]$ we have: – $I^{-1}\cap K[x]=(I:_{K(x)}I)$. – If there exists $p/q \in I^{-1}-K[x]$, then $(q,f)\neq 1$ in $K[x]$. If in addition $q$ is irreducible and $I$ is almost principal, then $I' = q(x)K[x] \cap R[x]$ is an almost principal upper to zero. Finally we show that a Schreier domain $R$ is a greatest common divisor domain if and only if every upper to zero in $R[x]$ contains a primitive polynomial.
Disordered motility is one of the most important pathogenic characteristics of functional dyspepsia (FD), although the underlying mechanisms remain unclear. Since the sympathetic system is important to the regulation of gastrointestinal motility, the present study aimed to investigate the role of norepinephrine (NE) and adrenoceptors in disordered gastric motility in a rat model with FD. The effect of exogenous NE on gastric motility in control and FD rats was measured through an organ bath study. The expression and distribution of β-adrenoceptors were examined by real-time PCR, Western blotting and immunofluorescence. The results showed that endogenous gastric NE was elevated in FD rats, and hyperreactivity of gastric smooth muscle to NE and delayed gastric emptying were observed in the rat model of FD. The mRNA levels of β1-adrenoceptor and norepinephrine transporter (NET) and the protein levels of β2-adrenoceptor and NET were increased significantly in the gastric corpus of FD rats. All three subtypes of β-adrenoceptors were abundantly distributed in the gastric corpus of rats. In conclusion, the enhanced NE and β-adrenoceptors and NETs may be contributed to the disordered gastric motility in FD rats.
Genes encoding enzymes involved in fatty acids (FA) and glucose oxidation are transcriptionally regulated by peroxisome proliferator-activated receptors (PPAR), members of the nuclear receptor superfamily. Under conditions associated with O 2 deficiency, PPAR-α modulates substrate switch (between FA and glucose) aimed at the adequate energy production to maintain basic cardiac function. Both, positive and negative effects of PPAR-α activation on myoc ardial ischemia/reperfusion (I/R) injury have been reported. Moreover, the role of PPAR-mediated metabolic shifts in cardioprotective mechanisms of preconditioning (PC) is relatively less investigated. We explored the effects of PPAR-α upregulation mimicking a delayed “second window” of PC on I/R injury in the rat heart and potential downstream mechanisms involved. Pretreatment of rats with PPAR-α agonist WY-14643 (WY, 1 mg/kg, i.p.) 24 h prior to I/R reduced post-ischemic stunning, arrhythmias and the extent of lethal injury (infarct size) and ap optosis (caspase-3 expression) in isolated hearts exposed to 30-min global ischemia and 2-h reperfusion. Protection was associated with remarkably increased expression of PPAR- α target genes promoting FA utilization (medium-chain acyl-CoA de hydrogenase, pyruvate dehydrogenase kinase-4 and carnitine palmitoyltransferase I) and reduced expression of glucose transporter GLUT-4 responsible for glucose transport and metabolism. In addition, enhanced Akt phosphorylation and protein levels of eNOS, in conjunction with blunting of cardioprotection by NOS inhibitor L-NAME, were observed in the WY-treated hearts. Conclusions: upregulation of PPAR-α target metabolic genes involved in FA oxidation may underlie a delayed phase PC-like protection in the rat heart. Potential non-genomic effects of PPAR-α-mediated cardioprotection may involve activation of prosurvival PI3K/Akt pathway and its downstream targets such as eNOS and subsequently reduced apoptosis., T. Ravingerová ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy