Null systems in the non-minimal case

In this paper, it is shown that if a dynamical system is null and distal, then it is equicontinuous. It turns out that a null system with closed proximal relation is mean equicontinuous. As a direct application, it follows that a null dynamical system with dense minimal points is also mean equicontinuous. Meanwhile, a distal system with trivial $\text{Ind}_{\text{fip}}$-pairs and a non-trivial regionally proximal relation of order $\infty$ are constructed.

Topological Sequence Entropy and Chaos

A dynamical system is called a null system, if the topological sequence entropy along any strictly increasing sequence of non-negative integers is 0. Given 0 ≤ p ≤ q ≤ 1, a dynamical system is [Formula: see text] chaotic, if there is an uncountable subset in which any two different points have trajectory approaching time set with lower density p and upper density q. It shows that, for any 0 ≤ p < q ≤ 1 or p = q = 0 or p = q = 1, a dynamical system which is null and [Formula: see text] chaotic can be realized.

Intramyocardial pressure measurements in the stage 18 embryonic chick heart

Intramyocardial pressure (IMP) and ventricular pressure (VP) were measured in the trabeculating heart of the stage 18 chick embryo (3 days of incubation). Pressure was measured at several locations across the ventricle using a fluid-filled servo-null system. Maximum systolic and minimum diastolic IMP tended to be greater in the dorsal wall than in the ventral wall, but transmural distributions of peak active (maximum minus minimum) IMP were similar in both walls. Peak active IMP near midwall was similar to peak active VP, but peak active IMP in the subepicardial and subendocardial layers was four to five times larger. These results suggest that the passive stiffness of the dorsal wall is greater than that of the ventral wall and that during contraction the inner and outer layers of both walls generate more contractile force and/or become less permeable to flow than the middle part of the wall. Measured pressures likely correspond to regional variations in wall stress that may influence morphogenesis and function in the embryonic heart.

An Active Control Design for a Class of Parametrically Excited Systems Based on the Gradient Algorithm

This paper introduces a new control design for a dynamic system subject to stationary or nonstationary parametric excitations. In this new design, the system dynamics is transformed into one with a null system matrix using the variation of parameters method. A stabilizing state feedback control can then be immediately obtained by following the gradient algorithm that is originally developed for the parameter identification purpose. Such a design has the advantage that the control requires only past and present information of the time-varying parametric excitations while previous control designs usually require prediction of future information of the excitations. The closed-loop system stability is guaranteed if the open-loop state response does not diverge too fast. The control design approach can also be applied to the observer design in case where there is only partial observation of the system state.

Fluid exchanges across the parietal peritoneal and pleural mesothelia

In 31 anesthetized rabbits, after removal of superficial tissues, glass micropipettes filled with 0.5 M NaCl solution and connected to an electrohydraulic servo-null system were used to measure extraperitoneal interstitial fluid pressure (Pi,per) and peritoneal liquid pressure (Pliq,per) at various heights. Linear regressions relating pressure to recording height (H) were Pi,per = 1.07 – 0.27H and Pliq,per = 0.9 – 0.64H, respectively. Protein concentration (Cp;g/dl) and colloid osmotic pressure (II; cmH2O) of plasma and of peritoneal and pleural liquids were 5.48 +/- 0.38 and 24.61 +/- 3.23, 3.07 +/- 0.5 and 13.29 +/- 1.87, and 1.76 +/- 0.42 and 8.45 +/- 2, respectively. The equation relating II to Cp was II = 4.64Cp + 0.0027Cp2. Tissue fluid samples were collected with saline-soaked wicks implanted in vivo or dry wicks inserted postmortem in extraperitoneal and extrapleural interstitial spaces. After 60 and 15 min, respectively, wicks were withdrawn and centrifuged; wick fluid was analyzed in colloid osmometer for small samples. Average extraperitoneal and extrapleural II values were 14.2 +/- 2.49 and 11.94 +/- 1.52 cmH2O, corresponding to Cp of 3.07 and 2.57 g/dl, respectively. The average net pressure gradient, assuming reflection coefficient and hydraulic conductivity (Negrini et al. J. Appl. Physiol. 69: 625–630, 1990; 71: 2543–2547, 1991), was 1.18 and 0.98 cmH2O for parietal peritoneal and pleural mesothelia, respectively, favoring filtration from the extraserosal interstitia into the serosal cavities. Total parietal peritoneal filtration was 1.49 ml.kg-1.h-1, approximately 15-fold higher than that for pleural mesothelium.

Microvascular pressure profile in intact in situ lung

We measured the microvascular pressure profile in lungs physiologically expanded in the pleural space at functional residual capacity. In 29 anesthetized rabbits a caudal intercostal space was cleared of its external and internal muscles. A small area of endothoracic fascia was surgically thinned, exposing the parietal pleura through which pulmonary vessels were clearly detectable under stereomicroscopic view. Pulmonary microvascular pressure was measured with glass micropipettes connected to a servo-null system. During the pressure measurements the animal was kept apneic and 50% humidified oxygen was delivered in the trachea. Pulmonary arterial and left atrial pressures were 22.3 +/- 1.5 and 1.6 +/- 1.5 (SD) cmH2O, respectively. The segmental pulmonary vascular pressure drop expressed as a percentage of the pulmonary arterial to left atrial pressure was approximately 33% from pulmonary artery to approximately 130-microns-diam arterioles, 4.5% from approximately 130- to approximately 60-microns-diam arterioles, approximately 46% from approximately 60-microns-diam arterioles to approximately 30-microns-diam venules, approximately 9.5% from 30- to 150-microns-diam venules, and approximately 7% for the remaining venous segment. Pulmonary capillary pressure was estimated at approximately 9 cmH2O.

Effect of chronic verapamil treatment on ventricular function and growth in chick embryos

Adjustment of myocardial mass to work load is a fundamental characteristic of the heart. We studied the effect of verapamil, a calcium channel blocker, on growth and function of chick embryonic ventricle. We treated stage 18 chick embryos with verapamil delivered to the extraembryonic vascular bed by a miniosmotic pump and compared them with saline-treated control and untreated embryos. At stages 24, 27, and 29, we measured ventricular pressure and dP/dt by a servo-null system, dorsal aortic stroke volume and dV/dt by pulsed-Doppler, and ventricular and embryo wet weights. Mean myocyte profile area was measured by digital planimetry technique, and cell growth response by DNA and protein assay. Verapamil treatment decreased ventricular pressure in experimental (P less than 0.05) compared with saline control and normal embryos; at stage 27, 1.59 +/- 0.21 vs. 2.17 +/- 0.05 and 2.35 +/- 0.08 (SE) mmHg, respectively. Mean dorsal aortic blood flow decreased in experimental (P less than 0.05) vs. control and normal embryos; at stage 27, 0.98 +/- 0.07 vs. 1.54 +/- 0.10 and 1.56 +/- 0.07 mm3/s, respectively. Stroke volume remained the same in all experimental, normal, and control embryos except at stage 29. Ventricular weight decreased in experimental (P less than 0.05) vs. control and normal embryos; at stage 27, 1.09 +/- 0.07 vs. 1.51 +/- 0.08 and 1.54 +/- 0.11 mg, respectively. Embryo weights, myocyte size, and cytoplasmic fractional volume were similar in all groups. Morphology of ventricles was normal. DNA was lower in experimental (P less than 0.05) compared with control and normal embryos.(ABSTRACT TRUNCATED AT 250 WORDS)

Control of bat wing capillary pressure and blood flow during reduced perfusion pressure

Regulation of blood flow depends on changes in the sum of arterial (Ra) and venous (Rv) resistances, whereas regulation of capillary pressure (Pc) depends on the ratio of Rv to Ra. If the myogenic response of the arterial system (i.e., delta Ra) is the primary mechanism for controlling pressure and flow when perfusion pressure is lowered, then Pc and total flow should be regulated to the same degree under these conditions. This hypothesis was tested by making direct measurements of Pc and flow in skin and skeletal muscle in the wings of unanesthetized bats. The box method was used to reduce perfusion pressure to the wing. Pressures were measured with a servo-null system; flows were computed from measurements of vascular diameters and red cell velocities using intravital microscopy. All branching orders of arterioles dilated significantly during decreases in box pressure (Pb). For 0 less than Pb less than or equal to -30 mmHg, total flow (1st-order arteriolar flow) remained nearly constant, whereas Pc was "regulated" only approximately 60%. These results cannot be explained by changes in arteriolar resistance alone and suggest that changes in Rv may be important. The possible consequences of flow redistribution, capillary recruitment, and micropressure sampling procedures are discussed in relationship to local regulation of capillary pressure and flow.