The evolution of chemical patterns in reactive liquids, driven by hydrodynamic instabilities.

We summarize our activity in unveiling a very wide phenomenon: When a chemical reaction takes place at a liquid interface, spectacular patterns of product form (see Plate 1). The pattern formation phenomenon is general, and is observed in reactions between liquids separated by a membrane, in liquids subjected to gaseous reactants, and in photoreactive liquids. We have demonstrated the phenomenon on over 100 different reactions of all types, thus discovering what we believe to be one of the widest macroscopic pattern formation processes known to chemistry. As can be seen in the accompanying pictures, the richness, beauty, and variations in types of patterns can be breathtaking. Two important aspects of these patterns are noted: First, the patterns are true far-from-equilibrium structures, which are maintained only as long as reactants are available, or only as long as light energy is supplied to the system; and second, the chemical products that form the patterns are not precipitates, but are entirely soluble in the liquid in which they form. Thus, if the containers in which the patterns form are shaken or stirred, a homogeneous solution results. Our research of this phenomenon concentrated on three main aspects. The first one was phenomenological. Here we explored the scope and generality of the phenomenon, motivated both by the aesthetic appeal of the phenomenon, and by the puzzle of how is it that such a wide-scope, experimentally simple phenomenon, has by and large, escaped the attention of the scientific community.The second aspect was devoted to the understanding of the underlying general mechanism. Of the many mechanisms we analyzed and tested, some very complex, others quite trivial, the one that fits the majority of the physical and chemical observations is the following: By performing a reaction through a liquid interface, a concentration gradient of the product forms near the interface. We have shown that in many cases, these gradients lead to hydrodynamic instabilities, which then break nonlinearly into a pattern which onsets slow convections. In other words, we found that these patterns mark the route along which a chemical instability relaxes. The third aspect of our research was theoretical. Here we concentrated in depth on one of the reactions (the Fe(+2)/Fe(+3) photoredox reaction), determined all its important physical parameters, and modeled its behavior theoretically. Our model, which was based on the instability buildup described above, was solved numerically, and its results compared with computerized image analysis of the evolving patterns; very good agreement between theory and experiment, was obtained. (c) 1995 American Institute of Physics.

Development of immature stomata: evidence for epigenetic selection of a spacing pattern.

In Sansevieria trifasciata as many as half the potential stomata remain immature. The development of all stomatal structures started at the same time and the early stages of the development of immature stomata had no special characteristics. Statistical analysis showed that the mature stomata were more evenly spaced than all potential stomata, both mature and immature. Furthermore, the distribution of mature stomata per unit area was more predictable or orderly than comparable structures of a random model that developed in the same way. These facts indicate that a nonrandom loss of many stomata by "immaturity" is a major determinant, acting during rather than preceding development, of the distribution of the mature, functional stomata. Thus in Sansevieria there is a selection of an epidermal pattern from an excess of cells that undergo the early stages of stomatal development.

Geometric phase shifts in chemical oscillators.

One of the most remarkable developments in quantum mechanics in recent years has been the discovery that when a system is moved adiabatically around a closed loop in parameter space there occurs, besides the familiar dynamical phase shift, an additional phase shift (sometimes referred to as 'Berry's phase') that is purely geometric in nature. The dynamical phase shift, which results from the variation of the period of the oscillatory system with the change in parameters, is relatively easily understood and is proportional to the time over which the parameter change occurs. The geometric phase shift, on the other hand, is less intuitive and depends on the curvature of the surface in parameter space bounded by the closed path, but is independent of the time taken to traverse the circuit. Here we present evidence for time-independent geometric phase shifts in numerical solutions for a model of an oscillating chemical reaction. The conditions for the occurrence of such shifts seem to be sufficiently general that geometric phase effects should be experimentally observable in essentially all chemical oscillators as well as in biological networks such as the brain and the central nervous system, where phase control is of vital importance.

Studies of arterial smooth muscle relaxation in younger (16-18 week) and older (28-31 week) spontaneously hypertensive rats.

Both isometric and isotonic relaxation rates have previously been reported to be decreased in caudal arterial and mesenteric resistance arterial smooth muscle from 16- to 21-week-old spontaneously hypertensive rats (SHR) compared with muscle from age-matched normotensive Wistar-Kyoto rats (WKY). An increased maximum velocity of shortening (Vmax) and an increased shortening ability (delta Lmax) have also been reported for arterial smooth muscle from 16- to 21-week-old SHR. It has been suggested that both increased narrowing and prolonged narrowing of arteries contribute to the development of hypertension. However, SHR Vmax is not different from WKY Vmax when studying arterial muscle from older (28- to 31-week-old) rats. Thus increased arterial narrowing ability cannot be a contributing factor to the maintenance of hypertension. In this study the role of relaxation rate in the maintenance of hypertension was examined by comparing the relaxation rates of isometric and isotonic contractions of caudal arterial strips from 16- to 21-week-old SHR (n = 9) and WKY (n = 8) and from 28- to 31-week-old SHR (n = 7) and WKY (n = 5). While relaxation rates were lower for 16- to 21-week-old SHR compared with age-matched WKY preparations for both isometric and isotonic contractions, only isometric relaxation rates were found to be different in 28- to 31-week-old SHR compared with 28- to 31-week-old caudal arterial muscle (p less than 0.05). Vmax tended to normalize from a once-elevated velocity, while isometric relaxation rate remained decreased in SHR with ageing and (or) with progression of the hypertensive condition.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of 2,3-butanedione monoxime (BDM) on smooth muscle mechanical properties.

2,3-Butanedione monoxime (BDM) has been reported to selectively block crossbridge interaction in skeletal and cardiac muscle and BDM has been shown to cause a dose-dependent decrease in smooth muscle maximum tension development (Po). With the relatively recent descriptions of at least two functionally different types of crossbridges (those recruited early in contraction and then fairly rapidly--within 30% of the muscles' contraction time--replaced by very slowly-cycling or "latch" crossbridges), it became important to know whether BDM is a specific inhibitor of one type of crossbridge or the other. In this study it was shown that 7.5 mM BDM had an even greater affect on maximum shortening ability (delta Lmax) having decreased the tracheal smooth muscle delta Lmax by 47%. BDM treatment did not alter "transition time (tT; defined arbitrarily as the time in contraction at which a functionally significant number of slowly-cycling bridges have replaced rapidly-cycling bridges)" in tracheal smooth muscle. Velocity of shortening early in contraction i.e. prior to tT, was decreased by 48%, while velocity late in contraction i.e. post tT, was not decreased with BDM treatment. BDM caused a decrease in maximum load bearing capacity, or maximum force potential (MFP), at all times in contracting tracheal smooth muscle. This investigation supports the suggestion that BDM inhibits crossbridge cycling rate in smooth muscle. In particular BDM appears to specifically inhibit rapidly-cycling crossbridges or their control as it has no apparent affect on cycling rate of very slowly-cycling or "latch" crossbridges in tracheal smooth muscle.

Time dependence of shortening velocity in tracheal smooth muscle.

It seems fairly well established that in the early phase of smooth muscle contraction cross bridges cycle at a relatively rapid rate. Later on these are replaced by very slowly cycling cross bridges or "latch bridges," operating with high economy. We describe a method to identify the time at which the transition occurs. By abruptly applying a light afterload at varying time intervals after stimulation of a canine tracheal smooth muscle, a point in time could be identified when cross-bridge cycling slowed. This was called the transition time. Because this transition was load dependent, the study was repeated with the preload abruptly reduced to zero. This permitted analysis of data in terms of cross-bridge activity. Maximum zero load velocity (Vo) of the contractile machinery was plotted against time and yielded a biphasic curve. The descending limb of the curve was fitted by a curve of the form Vo(t) = alpha e-K1t + beta e-K2t; K1 was almost three times greater than K2. We speculate that the faster rate constant represented activity of the early rapidly cycling cross bridges, and the slower constant reflected cycling rates in the latch state. These results are consistent with the latch bridge hypothesis put forward by Dillon et al. and enable us to provide a first approximation of the relative velocities of the two types of cross bridges.

Decreased velocity of shortening in arterial smooth muscle from older (28- to 31-week-old) spontaneously hypertensive rats.

An increased maximum velocity of shortening (Vmax) and increased shortening ability (delta Lmax) have been reported for caudal arterial smooth muscle from 16- to 18-week-old spontaneously hypertensive rats (SHR) compared with age-matched Wistar-Kyoto (WKY) control rats. It is known that hypertension results in hypertrophy of vascular smooth muscle. It is plausible that the faster Vmax of 16- to 18-week-old SHR arterial smooth muscle may slow down with age due to hypertrophy. The force-velocity (F-V) study done previously on caudal arterial strips from 16- to 18-week-old SHR and WKY rats was repeated on preparations from 28- to 31-week-old rats. An electromagnetic muscle lever was employed in recording force-velocity data. Analysis of these data revealed that the 28- to 31-week-old SHR (n = 7) mean F-V curve was not different from the 28- to 31-week-old WKY (n = 5) mean F-V curve (p greater than 0.05), and the shortening ability of 28- to 31-week-old SHR arterial muscle was significantly depressed compared with 28- to 31-week-old WKY arterial muscle (p less than 0.01). In conclusion, (i) although Vmax is faster in younger (16- to 18-week-old) SHR compared with age-matched WKY caudal arterial smooth muscle, SHR Vmax is not different from WKY Vmax in the older (28- to 31-week-old) rats. (ii) Shortening ability is greater in 16- to 18-week-old SHR caudal arterial strips compared with 16- to 18-week-old WKY strips, but is significantly depressed in 28- to 31-week-old SHR compared with 28- to 31-week-old WKY preparations.(ABSTRACT TRUNCATED AT 250 WORDS)