Flow limitation in liquid-filled lungs: effects of liquid properties

Flow limitation in liquid-filled lungs is examined in intact rabbit experiments and a theoretical model. Flow limitation ("choked" flow) occurs when the expiratory flow reaches a maximum value and further increases in driving pressure do not increase the flow. In total liquid ventilation this is characterized by the sudden development of excessively negative airway pressures and airway collapse at the choke point. The occurrence of flow limitation limits the efficacy of total liquid ventilation by reducing the minute ventilation. In this paper we investigate the effects of liquid properties on flow limitation in liquid-filled lungs. It is found that the behavior of liquids with similar densities and viscosities can be quite different. The results of the theoretical model, which incorporates alveolar compliance and airway resistance, agrees qualitatively well with the experimental results. Lung compliance and airway resistance are shown to vary with the perfluorocarbon liquid used to fill the lungs. Surfactant is found to modify the interfacial tension between saline and perfluorocarbon, and surfactant activity at the interface of perfluorocarbon and the native aqueous lining of the lungs appears to induce hysteresis in pressure-volume curves for liquid-filled lungs. Ventilation with a liquid that results in low viscous resistance and high elastic recoil can reduce the amount of liquid remaining in the lungs when choke occurs, and, therefore, may be desirable for liquid ventilation.     

Density dependence of maximal expiratory flow before and during tracheal constriction in dogs

The effect of carbachol-induced central bronchoconstriction on density dependence of maximal expiratory flow (MEF) was assessed in five dogs. MEFs were measured on air and an 80% He-20% O2 mixture before and after local application of carbachol to the trachea. Airway pressures were measured using a pitot-static probe, from which central airway areas were estimated. At lower concentrations of carbachol the flow-limiting site remained in the trachea over most of the vital capacity (VC), and tracheal area and compliance decreased in all five dogs. In four dogs, decreases in choke point area predominated and produced decreases in flows. In one dog the increase in airway "stiffness" apparently offset the fall in area to account for an increase in MEF. Density dependence measured as the ratio of MEF on HeO2 to MEF on air at 50% of VC increased in all five dogs. Increases in density dependence appeared to be related to increases in airway stiffness at the choke point rather than decreases in gas-related airway pressure differences. Lower concentrations produced a localized decrease in tracheal area and extended the plateau of the flow-volume curve to lower lung volumes. Higher concentrations caused further reductions in tracheal area and greater longitudinal extension of bronchoconstriction, resulting in upstream movement of the site of flow limitation at higher lung volumes. Density dependence increased if the flow-limiting sites remained in the trachea at mid-VC but fell if the flow-limiting site had moved upstream by that volume.     

Interdependent regional lung emptying during forced expiration: a transistor model

We recognized similarities between isovolume pressure-flow curves of the lung and emitter-collector voltage-current characteristics of bipolar transistors, and used this analogy to model expiratory flow limitation in a two-generation branching network with parallel nonhomogeneity. In this model, each of two bronchi empty parenchymal compliances through a common trachea, and each branch includes resistances upstream and downstream of a flow-limiting site. Properties of each airway are specified independently, allowing simulation of differences between the tracheal and bronchial generations and between the parallel bronchial paths. Simulations of four types of parallel asymmetry were performed: unilateral peripheral bronchoconstriction; unilateral central bronchoconstriction; asymmetric redistribution of parenchymal compliance; and unilateral alteration of the bronchial area-transmural pressure characteristic. Our results indicate that multiple axial choke points can exist simultaneously in a symmetric lung when large airway opening-pleural pressure gradients exist; despite severe nonhomogeneity of regional lung emptying, flow interdependence among parallel branches tends to maintain a near normal configuration of the overall maximal expiratory flow-volume (MEFV) curve throughout a large fraction of the vital capacity; and sudden changes of slope of the MEFV curve ("knees" or "bumps") may reflect choking in one branch in a nonuniform lung, but need not be obvious even when severe heterogeneity of lung emptying exists.     

The delay phenomenon: the story unfolds

Our previous studies have shown that when a flap is delayed, there is dilation of existing vessels within the flap not ingrowth of new vessels. The maximal anatomic effect on the arterial tree occurs at the level of the reduced-caliber "choke" anastomotic vessels that link adjacent vascular territories. To further investigate the sequence of anatomic changes that occurs during the delay phenomenon, a large series of 200 rabbits and 17 dogs underwent a flap delay procedure in either skin or muscle and the tissues were examined at postoperative periods between 1 hour and 1 year by using well-established fluorescein, angiographic, light microscopic, immunohistochemical, and electron microscopic techniques. These data in the rabbit skin consistently demonstrated an initial period of vasoconstriction that resolved within 3 hours postoperatively and was followed by an active and progressive dilation of choke vessels that was most dramatic between 48 and 72 hours. In vivo intravenous fluorescein dye testing revealed an interesting parallel in that there was a temporary barrier to the flow of fluorescein that occurred at the level of the choke vessels immediately after the flap was raised and that this temporary barrier-continued to impede the flow toward the flap tip in rabbits where flaps had been delayed for periods up to 72 hours. Thereafter, there was no obstruction to the flow of fluorescein along the flap. During this early delay period of 3 days, light microscopy revealed a decrease in vessel wall thickness associated with an increase in lumen diameter. Over the next 4 days, the luminal diameter continued to dilate to a lesser extent and the vessel wall thickened. Immunohistochemical analysis showed increased cell division, maximal between 24 and 72 hours, in all layers of the choke vessel wall. During this same postoperative interval, transmission electron microscopy revealed phenotypic changes in smooth muscle cells from contractile to synthetic cells. Hypertrophy of the smooth muscle cells was also observed. The vascular endothelium, which initially showed evidence of denudation, was restored to a healthy intact appearance within the first week after delay. When followed for longer periods, long-term studies of the delayed flap of up to 1 year demonstrated dramatically a permanent dilation of the choke vessel lumen and a thickening of the choke vessel wall. In canine studies, one rectus abdominis muscle was delayed by ligating the deep inferior epigastric artery. The time sequence of choke vessel dilation, studied by sequential angiograms in vivo, was comparable to that of the rabbit skin model. To ascertain the permanence and irreversibility of this dilation, the normal circulation of the delayed rectus abdominis muscle was restored by reanastomosing the deep inferior epigastric artery. Even after a recovery period of up to 3 months, the choke vessels remained dilated and tortuous instead of reverting to their original narrow diameters. From this work, it is suggested that the choke vessel dilation seen in the delay period is a permanent and irreversible event. It is an active process associated with both an increase (hyperplasia) and an enlargement (hypertrophy) of the cells in all layers of the choke artery wall and a resultant increase in caliber of these vessels. The time sequence for delay appears to be similar in different species and in different tissues, suggesting the possibility of a universal process for delay.     

Modeling expiratory flow from excised tracheal tube laws.

Flow limitation during forced exhalation and gas trapping during high-frequency ventilation are affected by upstream viscous losses and by the relationship between transmural pressure (Ptm) and cross-sectional area (A(tr)) of the airways, i.e., tube law (TL). Our objective was to test the validity of a simple lumped-parameter model of expiratory flow limitation, including the measured TL, static pressure recovery, and upstream viscous losses. To accomplish this objective, we assessed the TLs of various excised animal tracheae in controlled conditions of quasi-static (no flow) and steady forced expiratory flow. A(tr) was measured from digitized images of inner tracheal walls delineated by transillumination at an axial location defining the minimal area during forced expiratory flow. Tracheal TLs followed closely the exponential form proposed by Shapiro (A. H. Shapiro. J. Biomech. Eng. 99: 126-147, 1977) for elastic tubes: Ptm = K(p) [(A(tr)/A(tr0))(-n) - 1], where A(tr0) is A(tr) at Ptm = 0 and K(p) is a parametric factor related to the stiffness of the tube wall. Using these TLs, we found that the simple model of expiratory flow limitation described well the experimental data. Independent of upstream resistance, all tracheae with an exponent n < 2 experienced flow limitation, whereas a trachea with n > 2 did not. Upstream viscous losses, as expected, reduced maximal expiratory flow. The TL measured under steady-flow conditions was stiffer than that measured under expiratory no-flow conditions, only if a significant static pressure recovery from the choke point to atmosphere was assumed in the measurement.     

Properties of steady maximal expiratory flow within excised canine central airways

Using our transistor model of the lung during forced expiration (J. Appl. Physiol. 62: 2013-2025, 1987), we recently predicted that 1) axially arranged choke points can exist simultaneously during forced expiration with sufficient effort, and 2) overall maximal expiratory flow may be relatively insensitive to nonuniform airways obstruction because of flow interdependence between parallel upstream branches. We tested these hypotheses in excised central airways obtained from five canine lungs. Steady expiratory flow was induced by supplying constant upstream pressure (Pupstream = 0-16 cmH2O) to the bronchi of both lungs while lowering pressure at the tracheal airway opening (16 to -140 cmH2O). Intra-airway pressure profiles obtained during steady maximal expiratory flow disclosed a single choke point in the midtrachea when Pupstream was high (2-16 cmH2O). However, when Pupstream was low (0 cmH2O), two choke sites were evident: the tracheal site persisted, but another upstream choke point (main carina or both main bronchi) was added. Flow interdependence was studied by comparing maximal expiratory flow through each lung before and after introduction of a unilateral external resistance upstream of the bronchi of one lung. When this unilateral resistance was added, ipsilateral flow always fell, but changes in flow through the contralateral lung depended on the site of the most upstream choke. When a single choke existed in the trachea, addition of the external resistance increased contralateral flow by 38 +/- 28% (SD, P less than 0.003). In contrast, when the most upstream choke existed at the main carina or in the bronchi, addition of the external resistance had no effect on contralateral maximal expiratory flow.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mechanism of reduced maximum expiratory flow in dogs with compensatory lung growth

We examined the mechanism of the reduced maximum expiratory flow rates (Vmax) in a dog model of postpneumonectomy compensatory lung growth. During forced expiration, a Pitot-static tube was used to locate the airway site of flow limitation, or choke point, and to measure dynamic intrabronchial pressures. The factors determining Vmax were calculated and the results analyzed in terms of the wave-speed theory of flow limitation. Measurements were made at multiple lung volumes and during ventilation both with air and with HeO2. Five of the puppies had undergone a left pneumonectomy at 10 wk of age, and 5 littermate controls had undergone a sham operation. All dogs were studied at 26 wk of age, at which time compensatory lung growth had occurred in the postpneumonectomy group. Vmax was markedly decreased in the postpneumonectomy group compared with control, averaging 42% of the control flow rates from 58 to 35% of the vital capacity (VC). At 23% of the VC, Vmax was 15% less than control. Choke points were more peripheral in the postpneumonectomy dogs compared with controls at all volumes. The total airway pressure was the same at the choke-point airway in the postpneumonectomy dogs as that in the same airway in the control dogs, suggesting that the airways of the postpneumonectomy dogs displayed different bronchial area-pressure behavior from the control dogs. Despite the decreased Vmax on both air and HeO2, the density dependence of flow was high in the postpneumonectomy dogs and the same as controls at all lung volumes examined.     

Insensitivity of maximum expiratory flow to bronchodilation in normal dogs

We examined the effects of the inhaled parasympatholytic agent atropine and the sympathomimetic agent salbutamol on partitioned frictional pressure (Pfr) losses to the site of flow limitation (choke point, CP) in dogs to see how changes brought about by these agents would affect maximum expiratory flow (Vmax) and response to breathing 80% He-20% O2 (delta Vmax) in terms of wave-speed theory of flow limitation. In open-chest dogs, a Pitot-static tube was advanced down the right lower lobe to locate CP, to determine CP lateral and end-on pressures (PE), and to partition the airway into peripheral (alveoli to sublobar) and central (sublobar to CP) segments. Measurements were obtained at approximately 50% vital capacity. After inhalation, CP locations were unchanged with both bronchodilating agents. After atropine inhalation, Pfr central was decreased by one-half compared with base line. Despite the decrease in Pfr central, however, Vmax failed to increase after atropine because of altered bronchial area pressure (BAP) behavior at the CP site. After salbutamol inhalation, Pfr peripheral was reduced by about one-half compared with base line. However, Vmax failed to increase, because this reduction was too small to significantly increase the CP pressure head (i.e., PE). delta Vmax was also insensitive to these agents. Our results show mechanisms by which small changes in Pfr, as well as the complex interaction of changes in Pfr and BAP, may limit the use of Vmax in detecting bronchodilation at different airway sites.     

Density dependence of maximal flow is lung volume dependent during bronchoconstriction

We examined the changes in maximum expiratory flow (Vmax) and the density dependence of maximum expiratory flow (delta Vmax) during histamine-induced bronchoconstriction in dogs. Histamine acid phosphate solution was nebulized into the airways of six dogs to produce predominantly peripheral airway obstruction. Vmax air, Vmax with the dogs breathing 80% He-20% O2 (delta Vmax), and airway sites of flow limitation (choke points) were examined at four lung volumes (VL), which ranged from 51 to 23% of the control vital capacity (VC). The findings were interpreted in terms of the wave-speed theory of flow limitation. At all VL, Vmax air decreased during bronchoconstriction by approximately 30% compared with the control value. Resistances peripheral to a 0.3-cm-diam airway were increased about threefold with histamine, whereas resistances between 0.6-cm-diam bronchi and main-stem bronchi increased just slightly. Airway diameters were measured in the air-dried lung at 20 cmH2O transpulmonary pressure. Our results showed that only at 44% VC did delta Vmax decrease in all experiments after histamine to indicate peripheral obstruction (mean: 68.5 to 45%). At 23% VC, delta Vmax increased slightly, from 22 to 28%. At 23 and 36% VC, substantial differences in the wave-speed variables between air and HeO2 were present before bronchoconstriction, so that delta Vmax was low in some dogs, although peripheral airway obstruction was not evident. When bronchoconstriction was produced, delta Vmax at 23% VC could not be decreased further and even increased in four of six dogs. Thus changes in delta Vmax at given lung volume may not reflect the predominant site of airflow obstruction during bronchoconstriction.     

新型小鼠跨区供血耳瓣模型的构建

目的：建立一个实时活体观察血管形态学变化小鼠跨区供血耳瓣模型。方法体重25～30 g清洁级ICR小鼠30只,双耳脱毛后,观察其血管分布情况。小鼠麻醉后,用眼科剪从尾侧向头侧剪断鼠耳基底部尾侧2/3,保留头侧1/3,形成耳前血管蒂跨三个血管体、二个choke区的耳瓣模型。将小鼠侧卧置于二维图像采集系统的动物承载台上,调节体视显微镜物镜并固定为25倍,设置步进参数,“弓”型路线渐次、局部采集造模后0,1,2,3,5,7,10,14,21,30 d的时间点图像,合成鼠耳全景图。重点观察皮瓣的坏死率、皮瓣内choke血管的形态学变化。结果 ICR小鼠耳有三个恒定的血管体来供养,从内到外依次为头侧血管体、中间血管体及尾侧血管体。术后5 d,耳瓣坏死面积趋于稳定,坏死率为（15±7）％。内侧血管体与中间血管体之间的choke动静脉的管径出现快速扩增,两者都在第10天左右达最大,choke静脉管径最高峰可达到原来的（3.9±0.5）倍,choke动脉管径最高峰可达到原来的（3.5±0.7）倍。10 d后,choke静脉管径开始减小,21 d后逐渐平稳,而choke动脉管径于术后10 d左右开始平稳,之后无明显减小。结论①跨区皮瓣切取后,静脉扩张是被动扩张,而动脉扩张是主动增值;②跨区皮瓣切取后血流动力学供区与潜力供区之间的choke区参与扩张的choke血管数量及扩张度均小于解剖供区与血流动力学供区之间的choke血管;③小鼠耳瓣模型为研究血管扩张机制及遴选促皮瓣存活药物的理想动物模型。     

Carbon accumulation in <Emphasis Type="Italic">Rhodotorula glutinis</Emphasis> induced by nitrogen limitation

Background

Oleaginous microorganisms, such as bacterium, yeast and algal species, can represent an alternative oil source for biodiesel production. The composition of their accumulated lipid is similar to the lipid of an oleaginous plant with a predominance of unsaturated fatty acid. Moreover this alternative to conventional biodiesel production does not create competition for land use between food and oleo-chemical industry supplies. Despite this promising potential, development of microbial production processes are at an early stage. Nutritional limited conditions, such as nitrogen limitation, with an excess of carbon substrate is commonly used to induce lipid accumulation metabolism. Nitrogen limitation implies modification of the carbon-to-nitrogen ratio in culture medium, which impacts on carbon flow distribution in the metabolic network.

Results

The goal of the present study is to improve our knowledge of carbon flow distribution in oleaginous yeast metabolism by focusing carbon distribution between carbohydrate and lipid pools in order to optimize microbial lipid production. The dynamic effects of limiting nitrogen consumption flux according to carbon flow were studied to trigger lipid accumulation in the oleaginous yeast Rhodotorula glutinis. With a decrease of the specific nitrogen consumption rate from 0.052 Nmol.Cmol_X^?1.h^?1 to 0.003 Nmol.Cmol_X^?1.h^?1, a short and transitory intracellular carbohydrate accumulation occurred before the lipid accumulation phase. This phenomenon was studied in fed-batch culture under optimal operating conditions, with a mineral medium and using glucose as carbon source. Two different strategies of decreasing nitrogen flow on carbohydrate accumulation were investigated: an instantaneous decrease and a progressive decrease of nitrogen flow.

Conclusions

Lipid production performance in these fed-batch culture strategies with R. glutinis were higher than those reported in the previous literature; the catalytic specific lipid production rate was 0.07 Cmol_lip.Cmol_X*^?1.h^?1. Experimental results suggested that carbohydrate accumulation was an intrinsic phenomenon connected to the limitation of growth by nitrogen when the nitrogen-to-carbon ratio in the feed flow was lower than 0.045 Nmol.Cmol^?1. Carbohydrate accumulation corresponded to a 440% increase of carbohydrate content. These results suggest that microbial lipid production can be optimized by culture strategy and that carbohydrate accumulation must be taken account for process design.

     

Body size,not maladaptive gene flow,explains death-feigning behaviour in <Emphasis Type="Italic">Timema cristinae</Emphasis> stick insects

Eco-evolutionary feedback loops, where rapid evolution influences the ecology of an organism and subsequently alters the evolutionary trajectory of the population, are intriguing possibilities, but evidence for or against them is scarce. Timema cristinae stick insects express variation within and among populations in the expression of death-feigning behaviour, but the causes of variation in this species is not known. Here, I test the hypothesis that variation in death feigning across populations stems from an eco-evolutionary feedback loop, whereby gene flow causes poor camouflage, which increases the strength of bird predation, and ultimately drives the evolution of increased death-feigning. By conducting behavioural trials on eight T. cristinae populations that differ in the degree of maladaptive gene flow incurred, I falsify the eco-evolutionary feedback hypothesis for the evolution of death-feigning. Instead, I show that smaller individuals are more likely to feign death than larger individuals. By rearing individuals in the lab, I offer suggestive evidence that the body size effect is explained by the age of wild-caught individuals: younger individuals feign death more than older individuals. These findings add an example to the literature where no eco-evolutionary feedback exists in a system for which other similar feedbacks have been found, and provide evidence that death-feigning behaviour depends on body size.     

Enzyme histochemical studies on the conducting system of the human heart

Summary In this communication, the results of applying various histochemical techniques for the localization of oxidoreductases, transferases, hydrolases and isomerases in the human heart are presented. The Purkinje fibres of the atrioventricular conducting system of the human heart differ from the myocardium proper in containing a slightly higher activity of most of the glycolytic and gluconeogenetic enzymes investigated. The relatively higher activity of 6-phosphofructokinase, the key enzyme in anaerobic carbohydrate metabolism, is especially noteworthy. On the other hand, the activities of some of the enzymes that play a part in the aerobic energy metabolism is slightly less than those in the myocardium fibres.As for the activity of the NADPH regenerating enzymes, the activity of 6-phosphogluconate dehydrogenase and malate dehydrogenase (oxaloacetate-decarboxylating) is somewhat higher, and the activity of glucose-6-phosphate dehydrogenase similar, in the Purkinje fibres compared to that in the myocardial fibres. The activity of myosin ATPase is similar for both types of fibre. Likewise, the fibres of the conducting system and of the myocardium show a similar activity of acid phosphatase, -glucuronidase, non-specific naphthylesterase and peroxidase. The neurogenic function of the conducting system of the human heart was demonstrated by the high activity of acetylcholinesterase in the Purkinje fibres and in the atrioventricular node. All these histochemical findings in Purkinje fibres are similar at widely differing levels of the conducting system.     

Flow characteristics of open vessels in zone 1 rabbit lungs

To describe the flow characteristics of vessels open in zone 1, we perfused isolated rabbit lungs with Tyrode's solution containing 1% albumin, 4% dextran, and papaverine (0.05 mg/ml). Lungs were expanded by negative pleural pressure (Ppl) of -10, -15, -20, and -25 cmH2O. Pulmonary arterial (Ppa) and venous (Ppv) pressures were varied relative to alveolar pressure (PA = 0) and measured 5-10 mm inside the pleura (i) and outside (o) of the lungs. With Ppa(o) at -2.5 cmH2O, we constructed pressure-flow (P-Q) curves at each Ppl by lowering Ppv(o) until Q reached a maximum, indicating fully developed zone 1 choke flow. Maximum flows were negligible until Ppl fell below -10 cmH2O, then increased rapidly at Ppl of -15 and -20 cmH2O, and at Ppl of -25 cmH2O reached about 15 ml.min-1.kg body wt-1. The Ppv(o) at which flow became nearly constant depended on degree of lung inflation and was 5-8 cmH2O more positive than Ppl. As Ppv(o) was lowered below Ppa(o), Ppv(i) remained equal to Ppv(o) until Ppv(i) became fixed at a pressure 2-3 cmH2O more positive than Ppl. At this point the choke flow was therefore located in veins near the pleural boundary. No evidence of choke flow (only ohmic resistance) was seen in the intrapulmonary segment of the vessels remaining open in zone 1. With Ppv(o) held roughly at Ppl, Q could be stopped by lowering Ppa(o), at which time Ppa(i) was several cmH2O above Ppv(i), showing that intrapulmonary vessel closure had occurred.(ABSTRACT TRUNCATED AT 250 WORDS)     

Bronchial mechanical properties and maximal expiratory flows

Flow limitation in a collapsible elastic tube is dependent on the area (A) vs. pressure (P) relationship (the "tube law") for the tube. In this paper, a tube law in which A varies as (1-P)-n1 at negative pressures is assumed. It is shown that wave-speed limitation is possible at negative pressures only if n1 is greater than 0.5. Dissipative limitation is also investigated. Viscous limitation can occur if n1 is greater than 0.5, and turbulent limitation can occur if n1 is not less than 0.4. For values of n1 less than 0.4, flow cannot be limited at negative pressures. Model simulations are used to show that a combination of a value of n1 less than 0.3 together with an area minimum in the bronchial tree produce a minimum (a "hook") in the flow-volume curve. In the vicinity of such hooks, density dependence exceeds the usually accepted theoretical maximum value. Simulations also show that, when n1 is sufficiently small, apparently supramaximal flows appear to be possible.     

Mechanism of lobar alveolar pressure decline during forced deflation in canine regional emphysema

Mink, S. N. Mechanism of lobar alveolar pressuredecline during forced deflation in canine regional emphysema.J. Appl. Physiol. 82(2): 632-643, 1997.A canine model of unilobar papain-induced emphysema was used toexamine the extent to which differences in alveolar pressures(PA) would develop between anemphysematous right lower lobe (RLL) and normal left lower lobe (LLL)during forced vital capacity (FVC) deflation. RLL and LLLPA(PA_RLL and PA_LLL,respectively) were measured by the alveolar capsule technique. Duringforced deflation, PA and lobarflows were determined between 95 and 20% FVC. A choke point common toboth lower lobes was observed at >40% FVC. The results showed thatdeflation compliance (C) was altered for the RLL such that <90%lobar vital capacity, C_RLL > C_LLL, whereas >90% lobar vitalcapacity, C_RLL < C_LLL. At 95 and 90% FVC, theinitial RLL PA decline wasgreater than that for the LLL (P < 0.05). However, large differences inPA were prevented because of theeffect of interdependence of regional expiratory flow (IREF). IREFcaused a relative decrease in RLL flows and increase in LLL flows thatlimited PA differences. Between 80 and 50% FVC, as C_RLL becamegreater than C_LLL, and because ofthe initial effect of IREF,PA_RLL was~PA_LLL.At 40% FVC, without IREF, lobar differences inPA widened. These findings indicate that IREF may affect the dynamics of flow limitation inregional lung disease.

     

Automatic drought stress detection in grapevines without using conventional threshold values

Aims

Because the water status of grapevines strongly affects the quality of the grapes and resulting wine, automated and early drought stress detection is important. Plant measurements are very promising for detecting drought stress, but strongly depend on microclimatic changes. Therefore, conventional stress detection methods require threshold values which define when plants start sensing drought stress. There is however no unique method to define these values. In this study, we propose two techniques that overcome this limitation.

Methods

Two statistical methods were used to automatically distinguish between drought and microclimate effects, based on a short preceding full-irrigated period to extract plant behaviour under normal conditions: Unfold Principal Component Analysis (UPCA) and Functional Unfold Principal Component Analysis (FUPCA). Both techniques aimed at detecting when measured sap flow rate or stem diameter variations in grapevine deviated from their normal behaviour due to drought stress.

Results

The models based on sap flow rate had some difficulties to detect stress on days with low atmospheric demands, while those based on stem diameter variations did not show this limitation, but ceased detecting stress when the stem diameter levelled off after a period of severe shrinkage. Nevertheless, stress was successfully detected with both approaches days before visible symptoms appeared.

Conclusions

UPCA and FUPCA based on plant indicators are therefore very promising for early stress detection.     

A Three‐Dimensionally Interconnected Carbon Nanotube–Conducting Polymer Hydrogel Network for High‐Performance Flexible Battery Electrodes

High‐performance flexible energy‐storage devices have great potential as power sources for wearable electronics. One major limitation to the realization of these applications is the lack of flexible electrodes with excellent mechanical and electrochemical properties. Currently employed batteries and supercapacitors are mainly based on electrodes that are not flexible enough for these purposes. Here, a three‐dimensionally interconnected hybrid hydrogel system based on carbon nanotube (CNT)‐conductive polymer network architecture is reported for high‐performance flexible lithium ion battery electrodes. Unlike previously reported conducting polymers (e.g., polyaniline, polypyrrole, polythiophene), which are mechanically fragile and incompatible with aqueous solution processing, this interpenetrating network of the CNT‐conducting polymer hydrogel exibits good mechanical properties, high conductivity, and facile ion transport, leading to facile electrode kinetics and high strain tolerance during electrode volume change. A high‐rate capability for TiO₂ and high cycling stability for SiNP electrodes are reported. Typically, the flexible TiO₂ electrodes achieved a capacity of 76 mAh g^–1 in 40 s of charge/discharge and a high areal capacity of 2.2 mAh cm^–2 can be obtained for flexible SiNP‐based electrodes at 0.1C rate. This simple yet efficient solution process is promising for the fabrication of a variety of high performance flexible electrodes.     

Enzyme histochemical studies on the Purkinje fibres of canine, bovine and porcine hearts

Synopsis Whereas in ungulates the Purkinje fibres of the atrioventricular conducting system are highly characteristic cells, those in the canine heart are poorly differentiated and accordingly they cannot always be readily identified in histological sections. Consequently in this paper the results of various histochemical tests on bovine and porcine hearts have been compared with the view of evaluating them as dependable methods for identifying Purkinje fibres that are microscopically poorly differentiated.It appeared that, histochemically, canine Purkinje fibres differ consistently in similar ways and as markedly from the common myocardial fibres as the morphologically typical conducting fibres in bovine and porcine hearts. The conducting fibres distinguish themselves from the myocardium proper in containing more glycogen and fewer lipids, in possessing higher activities of the enzymes -glucan phosphorylase,l-glycerol-3-phosphate:menadione oxidoreductase, myosin adenosine triphosphatase and monoamine oxidase, as well as in possessing lower activities of several dehydrogenases, cytochrome oxidase, peroxidase and mitochondrial adenosine triphosphatase. The relatively high activity of -glucan phosphorylase in particular is striking. As the activity of this enzyme persists during periods of up to 20 min after death, the staining method for this enzyme provides a valuable technique for identifying Purkinje fibres even if they are cytologically poorly differentiated.It is of interest in relation to electrophysiological data that the histochemical properties are similar in Purkinje fibres derived from widely differing levels of the conducting system. From the present histochemical findings it may be assumed that, as compared with the myocardium proper, the Purkinje fibres have a higher rate of anaerobic and a lower rate of aerobic metabolism. Furthermore, it is pointed out that histochemically the differences between Purkinje fibres and common myocardial cells on the one hand, and those between white (Type II) and red (Type I) striated muscle fibres on the other, are essentially similar.     

Numerical solutions for steady and unsteady flow in a model of the pulmonary airways

A computational model is presented for unsteady flow through a collapsible tube with variable wall stiffness. The one-dimensional flow equations are solved for inlet, outlet and external conditions that vary with time and for a tube with time-dependent, spatially-distributed local properties. In particular, the effects of nonuniformities and local perturbations in stiffness distribution in the tube are studied. By allowing the flow to evolve in time, asymptotically steady flows are calculated. When simulating a quasi-steady reduction in downstream pressure, the model demonstrates critical transitions, the phenomena of wave-speed limitation and the sites of flow limitation. It also exhibits conditions for which viscous flow limitation occurs. Computations of rapid, unsteady changes of the exit pressure illustrate the phenomena occurring at the onset of a cough, and the generation and propagation of elastic jumps.