Escherichia coli cad operon functions as a supplier of carbon dioxide.

Brain cells normally respond adaptively to bioenergetic challenges resulting from ongoing activity in neuronal circuits, and from environmental energetic stressors such as food deprivation and physical exertion. At the cellular level, such adaptive responses include the "strengthening" of existing synapses, the formation of new synapses, and the production of new neurons from stem cells. At the molecular level, bioenergetic challenges result in the activation of transcription factors that induce the expression of proteins that bolster the resistance of neurons to the kinds of metabolic, oxidative, excitotoxic, and proteotoxic stresses involved in the pathogenesis of brain disorders including stroke, and Alzheimer's and Parkinson's diseases. Emerging findings suggest that lifestyles that include intermittent bioenergetic challenges, most notably exercise and dietary energy restriction, can increase the likelihood that the brain will function optimally and in the absence of disease throughout life. Here, we provide an overview of cellular and molecular mechanisms that regulate brain energy metabolism, how such mechanisms are altered during aging and in neurodegenerative disorders, and the potential applications to brain health and disease of interventions that engage pathways involved in neuronal adaptations to metabolic stress.

Performance of bacterial strains used for distillery waste treatment on different substrates

The physiology and biochemistry of muskmelon (Cucumis melo L.) fruit were studied in combination with nitrogen and calcium nutrition. Two forms of nitrogen ((NH4)2SO4 and NH4NO3) and 2 sources of calcium (CaCO3 and CaCl2) were studied with particular reference to carbon dioxide and ethylene production. In addition, fruit ethanol, chlorine and sugar contents were also estimated. Calcium, when applied in the form of CaCl2, was detrimental, in that, it produced more carbon dioxide and ethylene, decreased the mean fruit weight and also advanced the respiration peak by about 2 days to the ninth day after harvest compared with the 11th day in CaCO3. In this case, very high fruit ethanol and chlorine content seemed to affect the fruit quality. Such detrimental results were not observed in CaCO3 treatments. Irrespective of the treatments, carbon dioxide and ethylene production curves followed a typical sigmoidal pattern, confirming the climacteric nature of the fruit. Carbon dioxide and ethylene production, total soluble solid and ethanol contents, and ethanol and chlorine contents were positively correlated. Carbon dioxide production and fruit weight, and fruit weight and chlorine content were negatively correlated.

Lysine decarboxylase of Escherichia coli has been the subject of enzymological studies, and the gene encoding lysine decarboxylase (cadA) and a regulatory gene (cadR) have been mapped. This enzyme is induced at low pH in the presence of lysine and achieves maximal level under anaerobic conditions. The induction of lysine decarboxylase increases the pH of the extracellular medium and provides a distinctive marker in tests of clinical strains. We report the sequence of the cad operon encoding lysine decarboxylase, a protein of 715 amino acids, and another protein, CadB, of 444 amino acids. The amino acid sequence of lysine decarboxylase showed high homology to that of the lysine decarboxylase of Hafnia alvei with less homology to the sequence of speC, which encodes the biosynthetic ornithine decarboxylase of E. coli. The cadA and cadB genes were separately cloned and placed under the control of lac and tac promoters, respectively, to facilitate independent study of their physiological effects. The cadB gene product had a mobility characteristic of a smaller protein on protein gels, analogous to that found for some other membrane proteins. The CadB sequence showed homology to that of ArcD of Pseudomonas aeruginosa, encoding an arginine/ornithine antiporter. Excretion studies of various strains, the coinduction of cadB and cadA, and the attractive physiological role for an antiport system led to a model for the coupled action of cadA and cadB in uptake of lysine, the reduction of H+ concentration, and excretion of cadaverine.

Thermodynamic analysis of syngas production via tri-reforming of methane and carbon gasification using flue gas from coal-fired power plants

Anaerobic Metabolism During Cardiopulmonary Bypass: Predictive Value of Carbon Dioxide Derived Parameters

Mayo Clinic, Rochester, Minnesota. roy.tk@mayo.eduCapnography: Clinical Aspects. Edited by J. S. Gravenstein, M.D., Dr. med. h.c., Michael B. Jaffe, Ph.D., and David A. Paulus, M.D. Cambridge, United Kingdom, Cambridge University Press, 2004. Pages: 441. Price: $120.00.Practicing anesthesiologists and intensivists have come to take capnography for granted in the monitoring of surgical and critically ill patients. Although many standard anesthesiology texts contain a chapter about this important and useful technique, a comprehensive up-to-date treatment of the subject is not easy to find. Capnography: Clinical Aspects fills this void.The book is a multiauthored effort edited by two academicians and an engineer working in industry. The editors acknowledge significant overlap between chapters and characterize the book as more of a “symposium” than a textbook. There is adequate continuity of style between chapters, but as with any book written in this format, some chapters are more interesting to read than others.The book is organized into four parts. The first part is meant to be clinical and describes the interaction of respiratory, cardiovascular, and metabolic systems in determining the amount of exhaled carbon dioxide as measured by capnography. This is followed by parts on basic carbon dioxide physiology, the history of capnography, and the technology of capnography.The clinical part is divided into four sections: Ventilation, Circulation, Metabolism, and Organ Effects. The ventilation section is further divided into subsections on breathing assessment, airway management, monitoring of ventilation, weaning, and special situations. The first chapter (written by two of the editors) is a well-written introduction to time-based capnogram interpretation, the most commonly used form of capnography in the operating room setting. Of particular value is the introduction to the volume-based capnogram, a topic not commonly detailed in anesthesia texts. Subsequent chapters discuss capnography outside the operating room and in the prehospital setting for airway management, in particular to confirm tracheal intubation. The chapter on airway management in the intensive care unit includes a section on using capnography to confirm proper orogastric and nasogastric tube placement. The chapter on airway management in the operating room includes sections on confirming tracheal intubation and recognizing endobronchial tube placement.The chapter describing the use of capnography to monitor ventilation during anesthesia includes interesting comments on the Food and Drug Administration checkout relevant to capnography. This chapter also includes sections on equipment troubleshooting and how capnograms can be affected by positioning, pulmonary pathology, and several particular situations such as one-lung ventilation, laparoscopy, neurosurgery, cardiac surgery, tourniquet release, and high-frequency jet ventilation. Other chapters in this section focus on the use of capnography during transport and how it can be used in the field as a way to avoid deleterious effects of unintentional hyperventilation after intubation.A particularly comprehensive chapter describes the unique physiology and technological limitations of capnography in neonates and infants. Other chapters describe capnography in the sleep laboratory, capnography as a feedback tool for behavioral therapy in various disorders, and how the capnogram is affected by alterations in physiologic and technical limitations in high- and low-pressure environments.Chapters are also included on sedation and noninvasive ventilation. These chapters are valuable for their descriptions of how end-tidal carbon dioxide can be sampled during spontaneous ventilation in nonintubated patients and the clinical utility and limitations of end-tidal carbon dioxide as a method of estimating arterial carbon dioxide tension (PCO2) in noninvasive ventilation.Chapters relevant to critical care describe the use capnography to optimize tidal volume, alveolar minute ventilation, and positive end-expiratory pressure to wean patients from mechanical ventilation. These chapters also describe the use of volumetric capnography to assess carbon dioxide production and how the capnogram is affected by positive end-expiratory pressure, unilateral lung injury, tracheal gas insufflation, and various high-frequency ventilation modes.The circulation subsection includes chapters on how end-tidal carbon dioxide monitoring can be used to assess circulatory status during cardiopulmonary resuscitation and for prognostication during cardiac arrest in medical patients as well as the use of end-tidal and tissue carbon dioxide monitoring techniques to assess oxygen delivery in shock states. This section includes an elegant physiologic description of changes in alveolar dead space with pulmonary embolism and the use of capnography in diagnosis and treatment of pulmonary emboli and gas embolization in addition to a chapter on the utility of volumetric capnography for estimating arterial PCO2in patients with acute respiratory distress syndrome.The chapter on noninvasive pulmonary blood flow measurement describes complete and partial carbon dioxide rebreathing techniques as alternatives to invasive cardiac output monitoring. A variety of clinical scenarios illustrating the use of these techniques sets this chapter apart from other descriptions of this topic.The metabolism subsection includes a single chapter describing alterations in normal physiology induced by surgery and anesthesia that affect carbon dioxide elimination. The chapter discusses alterations in ventilation, circulation, and carbon dioxide metabolism that are influenced by temperature alterations, various anesthetic techniques, and pharmacologic agents as well as particular intraoperative situations such as laparoscopy, tourniquet release, vascular cross clamping, and cardiopulmonary bypass.The final chapter of the ventilation section describes the effects of hypercapnia and hypocapnia on tissue oxygenation and perfusion, focusing on the central nervous system, respiratory system, and cardiovascular system. This is an excellent introduction to the effect of carbon dioxide at the organ, tissue, and cellular/molecular level and could have been included in the section on physiology.The physiology section includes a chapter on carbon dioxide pathophysiology, which describes inherited and acquired mitochondrial and enzyme disorders as well as pharmacologic agents that alter carbon dioxide production. The chapter also discusses carbon dioxide embolism and the increase in PCO2during apnea testing for brain death. There is a complete if somewhat standard chapter on acid–base physiology, followed by an excellent description of how capnography can provide information on ventilation/perfusion mismatch from a physiologic standpoint, including examples of various disease states. Subsequent chapters describe clinical correlates of alterations in normal time and volume capnographic tracings and how capnograms can provide clues to the underlying pathophysiology.A particularly interesting chapter in this section summarizes a biomedical engineering approach to illustrate the underlying anatomical and physiologic processes that result in a normal volumetric capnogram. A mathematical model that accounts for bronchial airway structure, gas convection and diffusion, and the carbon dioxide release from alveolar capillary blood is shown to generate a computed washout curve that shows remarkable agreement with an experimentally measured capnogram from a healthy human subject. This illustrates the utility of physiologic modeling as a useful tool for investigating potentially complex pathophysiologies without placing patients at risk.A unique historical section describes the evolution of time and volumetric capnography with many interesting anecdotes, as well as a first-person account by Smalhout, an early proponent of capnography. A selection of capnographic tracings corresponding to clinical events that he made over a 20-yr period is one of the highlights of this book. Without reading this section of the book, few people would realize that the impetus for carbon dioxide analyzer development was to investigate the cause of death in patients who turned out to be rebreathing due to a channeling issue through carbon dioxide absorption devices, or that carbon dioxide analyzers enabled a reduction in mortality for polio patients by allowing clinicians to titrate ventilation to expired carbon dioxide instead of adjusting ventilation based on their weight.The technological section fulfills the editors’ wishes for providing clinicians with information necessary to appreciate the mechanism, design, and limitations of devices for measuring carbon dioxide. Various chapters address technical specifications and standards (e.g. , accuracy, range, drift, response time, interfering gases, alarm systems, calibration) for carbon dioxide analyzers and describe technological limitations for flow measurement, required to estimate carbon dioxide production. Another chapter describes various methods for carbon dioxide detection, including infrared, photoacoustic, colorimetric, and mass spectrometry methods. Unfortunately, Raman spectroscopy is not included simply because it is not currently commercially available. This chapter also includes a discussion of mainstream versus sidestream carbon dioxide analyzers.The book ends with a mini-atlas of capnographic waveforms typifying various physiologic states, which is useful although not exhaustive.As the editors acknowledge, there is a fair amount of redundancy; as an example, the fact that highly sensitive colorimetric carbon dioxide indicators can yield false positives with esophageal intubation is mentioned in multiple chapters along with the fact that false negatives in cardiac arrest have led to the removal of correctly placed endotracheal tubes. Other recurring themes include the predictive value of end-tidal carbon dioxide in assessing arterial PCO2and the utility of volumetric capnography. In general, I found the multiple perspectives to be helpful instead of confusing or irritating. As with any book, the onus is on the reader to formulate his or her judgment with the assistance of the most recent literature.The overall introduction to the book and the introduction chapters for each section are very short and could have been used to provide the reader with a more substantial description of the basic concepts or objectives of each section. The section and subsection titles are somewhat arbitrary, and some chapters are in fact assigned to their own sections. Although the terminology is relatively consistent, the book could also use a more comprehensive list of abbreviations and acronyms used in various chapters. I found most of the typographical and page-setting errors to be minor (with the exception of a reference to “title” volumes). In spite of these limitations, the book admirably maintains its focus on capnography; readers interested in the latest tissue oxygen tension (PO2) monitoring techniques, for example, will have to look elsewhere.In summary, Capnography: Clinical Aspects is a very readable introduction to a topic addressed by few textbooks. It is useful as a reference primarily because of its comprehensive index and contains much information useful to the practitioner of critical care as well as anesthesiology. It addresses the physiologic and technological considerations that need to be understood to make capnography a clinically useful tool and should be standard reading for those who depend on it as a basic anesthetic monitor.Mayo Clinic, Rochester, Minnesota. roy.tk@mayo.edu

The effects of cell wall phenolics, lignins and fungal metabolites on end products of simulated rumen fermentations were studied. Monomeric phenolics, selected to represent the products of aerobic oxidation of lignin by fungi, slightly enhanced carbon dioxide output at low concentrations (0.05%) but had no stimulatory effect on acetate production. Higher concentrations (0.5%) of industrial and Klason lignin decreased carbon dioxide, methane, acetate and propionate production. Secondary metabolites from toxigenic strains of Aspergillus flavus, which were used to simulate the presence of contaminated feedstuff arising from non-sterile fungal bioconversion systems (fermentations), stimulated carbon dioxide, methane, acetate and propionate production but not when extracts were boiled or autoclaved. Acetate, propionate, methane and carbon dioxide production were only slightly reduced in the presence of purified aflatoxin. With spruce sawdusts pretreated with fungi, it was found that accumulation of soluble compounds from lignin and polysaccharide depolymerisations in rumen simulations were markedly higher with sawdusts pretreated with fungi under non-sterile conditions. It was concluded that fungal pretreatment of lignocellulosic substrates had no adverse effects on the end products of rumen fermentations.

The carbon dioxide produced by toad urinary bladders bathed on their mucosal surfaces by sodium Ringer solution and on their serosal surfaces by modified Leibovitz tissue culture medium was analysed by multiple regression on both sodium transport and time. The fractions contributed by metabolism related to transport and by basal metabolism were assessed, and the extent to which these might vary with time was determined. This analytical method, which improves the accuracy with which suprabasal metabolism is estimated, was used to examine the effects on metabolism of vasopressin, aldosterone, and mucosa-positive voltage-clamping. Vasopressin (0.05 u./ml), which on average increased sodium transport 2.9 times and concurrently increased the rate of carbon dioxide production in these transporting tissues, also altered the carbon dioxide production of non-transporting, amiloride-treated control hemibladders. For each hemibladder the ratio of sodium transported to suprabasal carbon dioxide produced after vasopressin was compared with that observed before vasopressin. Differences between the ratios were much reduced when the carbon dioxide productions of the paired transporting hemibladders were corrected for the effects of vasopressin on basal carbon dioxide production. With such analysis, it was confirmed that vasopressin did not alter the stoichiometry of sodium transport. A 30 mV, mucosa-positive voltage clamp, applied near the peak of the response to vasopressin, further increased both sodium transport and carbon dioxide production. No alterations of the ratio of sodium to suprabasal carbon dioxide were seen under these conditions where the maximal rate of active sodium transport in this tissue must have been approached. Active sodium transport was more than doubled some 4 h after adding aldosterone (10(-7) M). However, the related increase in suprabasal carbon dioxide production was greater than threefold. Therefore, whereas the stimulation resulting from vasopressin and voltage clamping had no effect on the ratio of sodium transported to suprabasal carbon dioxide produced, this ratio was reduced significantly by aldosterone. When the sodium transport of aldosterone-treated bladders was increased further by voltage clamping, the ratio of sodium transported to suprabasal carbon dioxide production remained at the reduced value. Sodium transport was increased by approximately 35% more when aldosterone-treated hemibladders were voltage clamped after vasopressin, the control paired hemibladders being exposed to vasopressin and voltage clamping alone.(ABSTRACT TRUNCATED AT 400 WORDS)

Methane (CH4) and carbon dioxide (CO2) production from six crossbred yearling beef heifers (400 ± 13.0 kg) were measured, using the sulphur hexafluoride (SF6) tracer gas technique (Tracer) and open-circuit hood calorimetry (Cal) to validate the former in estimating rumen CH4 and CO2 production in the field. Animals were individually fed a diet consisting of 50% barley concentrate and 50% alfalfa cubes at 1.3 &times ;maintenance requirements daily. Hifers were divided into two groups for individual animal 24- h gas measurements by each method. Each group of heifers was rotated between the Cal and Tracer techniques for 6 consecutive days in an incomplete block design. Methane production ranged from 108 to 145 L d-1 (mean 130 ± 4.0 L d-1) using the Cal technique, and 90 to 167 L d-1 (mean 137 ± 4.0 L d-1) using the Tracer technique. The mean CH4 production (L d-1) was not different (P = 0.24) between the two methods. Carbon dioxide production with the Tracer technique was 20% higher than CO2 production with the Cal technique (P < 0.01). The range of CO2 production was 1574 to 2049 L d-1 (mean 1892 ± 74.0 L d-1) by Cal, and 1541 to 3330 L d-1 (mean 2353 ± 74.0 L d-1) by Tracer. Day-to-day variation in CH4 production was not different within each method (P > 0.05); however, animal-to-animal variation (11.7%) was significant for the Tracer technique (P = 0.04), but not for the Cal technique (P = 0.53). Comparison of the equality of variance between the two methods showed that there were no differences in variations (P > 0.05) between Cal and Tracer for CH4 production. On the other hand, variations in CO2 production were not equal (P > 0.05) between methods. Day-to-day variation in CO2 production was significant using Cal, but not Tracer (P > 0.05). Animal-to-animal variation in CO2 production was 1.6 and 11.8% by Cal and Tracer techniques, respectively. It can be concluded that the SF6 tracer technique accurately estimated rumen CH4 production, but CO2 production was 20% higher. The study suggests that for CH4 measurements using the SF6 tracer technique, more animal numbers are needed than for Cal to reduce animal-to-animal variation. Key words: Methane, carbon dioxide, SF6 tracer technique, validation, cattle

Acute Responses of Functional Electrical Stimulation Cycling on the Ventilation-to-CO2 Production Ratio and Substrate Utilization After Spinal Cord Injury

Carbon dioxide is excreted by the lungs. Carbon dioxide production is based on metabolic rate and the substrates that are being utilized to drive the Kreb's cycle. Factors that influence pulmonary elimination of carbon dioxide include the volume of dead space, tidal volume, respiratory frequency and positive end-expiratory pressure (PEEP). The balance between arterial and venous carbon dioxide is based upon cardiac output. Hypocapnia can be controlled relatively through adjustment of ventilator settings to reduce minute ventilation in the sedated patient. The effects of hypercapnia and the associated acidaemia may be mitigated through the use of buffering agents. Traditionally, extracorporeal gas exchange (ECGE) has been utilized in patients only as a rescue therapy. In practice, clinicians adopt a technique somewhere between optimal carbon dioxide clearance and more liberal clearance targets, based on assessment of the severity of lung disease and the risks and benefits of ventilatory manipulations or associated interventions.

Ruminal fermentation produces greenhouse gases involved in global warming. Therefore, the effect of nutrient combinations on methane, carbon dioxide, and biogas production as well as ruminal fermentation kinetics was evaluated in in vitro studies. In total mixed rations, dietary corn grain was partially replaced by two levels of soybean hulls (a highly reusable residue), and a Moringa oleifera extract (a natural extract) at three concentration levels was added. Higher levels of both soybean hulls and M. oleifera extract delayed the initiation of methane production and resulted in a lower methane and carbon dioxide production. Thus, total biogas production was also lower. Replacement of corn grain by soybean hulls tended to lower methane production rates and asymptotic carbon dioxide production, and a delay in biogas and methane formation was observed. Asymptotic biogas and carbon dioxide production, however, were increased. The presence of M. oleifera extract tended to delay methane formation and to decrease methane production rate as well as asymptotic methane production. Higher M. oleifera extract levels decreased asymptotic biogas production with the control and the highest soybean hull levels. In the presence of M. oleifera extract, asymptotic carbon dioxide production was shown to be quadratically increased with the control and lowest soybean hull levels, but quadratically decreased with the highest soybean hull level. With the exception of fermentation pH, the interaction of substrate type and M. oleifera extract level was shown to have an effect on all fermentation parameters. Most fermentation parameters were shown to be higher when replacing corn grain by soybean hulls, including fermentation pH. Thus, the conclusion could be drawn that corn grain replacement by soybean hulls (an agricultural residue) in the presence of M. oleifera extract (a sparing leaf product) could ameliorate greenhouse gas emissions and improve digestion.

In 4 spontaneously breathing, barbiturate-anesthetized dogs, hyperthermia was induced with 2,4-dinitrophenol while rectal temperature, heart rate, mean blood pressure, end-tidal carbon dioxide, and carbon dioxide production (milliliters per minute) were measured continuously. The latter was determined with a pneumotachygraph (to obtain respired volume) and an infrared carbon dioxide analyzer that measured inspired and expired carbon dioxide concentration. Of the five physiologic measurements, the increase in carbon dioxide production preceded the increase in rectal temperature by more than 120 seconds. End-tidal carbon dioxide was an unreliable indicator in the spontaneously breathing animal of approaching hyperthermia during spontaneous breathing due to a transient tachypnea, which decreased end-tidal carbon dioxide. The carbon dioxide production (milliliters per minute) increased immediately and reached three to five times the control value. Blood pressure and heart rate were insensitive indicators of approaching hyperthermia.

During experiments upon the permeability of the yeast-cell it was found that, when yeast was immersed in a molar solution of sodium chloride, and allowed to stand at air temperature, the amount of gas produced by autofermentation was considerably greater than that given by a water control. The production of carbon dioxide by autofermentation of yeast is brought about by the action of at least two enzymes. The reserve material of the cell, for the most part glycogen, is first converted by a glycogenase into a sugar, which in turn is fermented by zymase with the production of alcohol and carbon dioxide. As the rate of autofermentation is considerably less than that produced by the same yeast in presence of excess of sugar, it follows that the rate of autofermentation is controlled by the rate of production of sugar within the cell, in other words, by the rate of action of the glycogenase. An increase in the rate of autofermentation, therefore, indicates greater activity of this enzyme within the cell. In order to investigate the action of solutions of various salts upon the rate of autofermentation of yeast, this was ascertained by measuring the volume of carbon dioxide evolved during successive intervals of time by means of the apparatus described by Harden, Thompson, and Young (1). The yeast employed was prepared from top-yeast as obtained from the brewery by pressing out the wort in a small hand press, it having been demonstrated (2) that practically the whole of the interstitial liquid can be removed in this way. A certain weight of such pressed yeast was carefully weighed into each of the fermentation flasks, and treated with a certain volume of the various liquids under experiment, controls being made with water. The liquids were saturated with carbon dioxide at 25°, the temperature of the water-bath.