scienceblogs.com — In most texts and sources that I've read, the germ theory of disease is stated something like, "Many diseases are caused by microorganisms." We could argue whether viruses count as microorganisms, but for purposes of the germ theory they do. (Most biologists do not consider viruses to be true living organisms, because they consist of nothing more than genetic material wrapped in a protein coat and lack the ability to reproduce without infecting the cell of an organism.) Now, let's take a look at the latest germ theory denialist idiocy I've come across. The first one, not surprisingly, I found on NaturalNews.com. Surprisingly, it was not written by Mike Adams, but rather by someone named Paul Fassa, who proclaims You have been lied to about germs. It should have been called "You are about to be lied to about germs." First, though, since this article wasn't by the usual science-hating loon Mike Adams, I was curious just who Paul Fassa is. I had never heard of him before. It didn't take long to find Fassa's Twitter account and then from there his blog Health Maven, which bills itself as an "escape from the medical mafia matrix." Interesting. Why does it appear that any time I come across a germ theory denialist like Fassa, he's someone who uses terms like "medical mafia matrix"? I don't know, but such people also tend to write introductory paragraphs like this: We have been taught to fear germs, pathogens, viruses, and bacteria that invade us from out there. This is the Pasteur model of disease contagion. This creates a dependency on Big Pharma to protect us from invading microbes, each having one form (monomorphic) and creating one specific disease. Pasteur`s model of disease won over rival Claude Bernard`s more accurate argument of the inner terrain. Pasteur`s declaration, though serving the coffers of Big Pharma, creates more questions: How come some get a disease that`s going around and others don`t? How do all these new bugs come out of nowhere to haunt us? Why do vaccines and antibiotics ultimately fail and create super bugs? These questions are answered by understanding the inner terrain and pleomorphism. Note how Fassa first misrepresents the Pasteur model of disease. This is common among germ theory denialists, in my experience. They tend to assume that germ theory states that pathogenic microbes are 100% infectious and always cause disease. Consequently, when people are exposed to pathogenic microbes and don't become ill, people like Fassa point to that as evidence that germ theory is invalid. After all, the germ didn't cause disease, at least in this one case! That must mean that all of germ theory is wrong! Concrete thinking, thy name is Fassa (and other germ theory denialists.) It's rather odd that even most teenagers can understand that catching an infectious disease is dependent not just on the microbe but each person's resistance to that microbe. This is the same thing that mystifies HIV/AIDS denialists, who seem to view the observation that most exposures to HIV do not result in AIDS as some sort of devastating indictment of the hypothesis that HIV causes AIDS. Add to that a long asymptomatic period and highly variable rates of progression, and HIV/AIDS denialists, who are--let's face it--really nothing more than a subtype of germ theory denialists who deny vehemently that one particular germ causes disease have all the doubt they need. But I digress. Also notice Fassa's early and immediate invocation of the pharma shill gambit. If there's another thing about germ theory denialism, it's that those who cling to it tend to be extremely distrustful of big pharma. I realize that in many cases big pharma deserves a lot of mistrust; its record in many areas demands it. What distinguishes many of these germ theory denialists is that they take healthy skepticism and take it to a pathological extreme. They also seem to think that the reason that antibiotics ultimately fail is because germ theory is invalid, which reveals an incredible ignorance of how antibiotics work. Helloooo! Evolution? Ever heard of it? Bacteria are incredibly good at evolving under the selective pressure of antibiotics. That's what creates superbugs, that and our tendency to overuse antibiotics. But what is the "inner terrain" and pleomorphism? This is where we find the "intellectual" basis of rejection of germ theory. As is the case with many alt-med beliefs, this basis harkens back to "ancient" knowledge (or at least 150 year old knowledge). It harkens back to Antoine Béchamp, who did indeed postulate nearly the exact opposite of what Pasteur did: that microorganisms were not the cause of disease but rather the consequence of disease, that injured or diseased tissues produced them and that it was the health of the organism that mattered, not the microorganisms. Basically, Béchamp's idea, known as the pleomorphic theory of disease, stated that bacteria change form (i.e., demonstrate pleomorphism) in response to disease, not as a cause of disease. In other words, they arise from tissues during disease states; they do not invade from the external world. Béchamp further proposed that bacteria arose from structures that he called microzymas, which to him referred to a class of enzymes. Béchamp postulated that microzymas are normally present in tissues and that their effects depended upon the cellular terrain. Ultimately, Pasteur's theory won out over that of Béchamp, based on evidence, but Béchamp was influential at the time. Given the science and technology of the time, Béchamp's hypothesis was not entirely unreasonable. It was, however, superseded by Pasteur's germ theory of disease and Koch's later work that resulted in Koch's postulates. What needs to be remembered is that not only did Béchamp's hypothesis fail to be confirmed by scientific evidence, but his idea lacked the explanatory and predictive power of Pasteur's theory. Fassa is sort of correct about one thing, though. Béchamp's idea was basically something like this: The inner terrain includes our immune system, organ tissues, and blood cells. Those who stepped out of line from Pasteur`s dogma asserted that the inner terrain was more vital for remaining disease free than searching for new antibiotics and vaccines to kill bacteria and viruses. As an analogy, flies don`t create garbage. But garbage attracts flies that breed maggots to create even more flies. Removing garbage is more effective than spraying toxic chemicals, which endanger human and animal life, around the house. Similarly, adding toxins to humans is not as effective as cleaning out the inner terrain. As I said, there's a grain of truth there, namely that the condition of the body and a person's immune system does matter. Specifically, it is true that the condition of the "terrain" (the body) does matter when it comes to infectious disease. Debilitated people do not resist the invasion of microorganisms as well as strong, healthy people. Of course, another thing to remember is that the "terrain" can facilitate the harmful effect of microorganisms in unexpected ways. For example, certain strains of the flu (as in 1918 and H1N1) are more virulent in the young because the young mount a more vigorous immune response. However, latter day Béchamp worshipers fetishize this idea to the point of claiming that the "inner terrain" is all that matters and that bacteria and viruses are manifestations, not causes, of disease. It goes beyond that, though. According to Béchamp, it's said: Blood is alive. It is not a liquid, but a mobile tissue (Béchamp was the first to describe blood thus). The things in our blood are alive. And one thing modern medicine does not accept is that something like a bacterium can change into a yeast that can turn into a fungus that can turn into a mold. We've talked about this in previous newsletters; it is called pleomorphism. Pleo meaning many and morph meaning form or body. This is, of course, complete nonsense. Bacteria cannot change into yeast or vice-versa, while yeasts are organisms in the kingdom Fungi. Dimorphic fungi can exist as a mold/hyphal/filamentous form or as yeast, but this fact does not invalidate the germ theory of disease. Indeed, some of these fungi are pathogens, such as Blastomyces dermatitidis, Histoplasma capsulatum, and Sporothrix schenckii. The misunderstanding of microbiology required to accept the rejection of germ theory in favor of Béchamp's ideas is staggering. Yet they remain very influential. Not among scientists, of course. Science moved on a long time ago. Rather, they remain influential among cranks. By Orac

discovermagazine.com — Thus passed the bulk of three years. Milton found that most of the time the howlers ate leaves and fruit in almost equal measure, but when seasonal fruits were in short supply, the animals filled up on leaves. Howler monkeys were finicky, though. They ate only tender, young leaves, and only the tips at that....They appear to use a collective information pool to locate their foods. They’ll just set off in a straight line right to it....The howlers conducted these expeditions over 75 acres, searching out as many as 25 species of plants daily. Some, like the Ceiba pentandra tree, were edible for only a few hours a year; others were available more often. Unerringly, the howlers tracked them down. The ranges of various howler troops overlapped, so Milton would occasionally come upon a tree filled with monkeys, with other groups in adjoining trees politely waiting their turn at the table. All of which suggested that the animals had an extraordinary collective memory, an unfailing sense of direction, refined social manners, and a built-in barometer of what foods were good for them.This aggregate intelligence allows infant howlers to mature quickly. After 12 to 14 months, howler mothers don’t want to see their babies again, Milton says. The babies soon declare independence and rely on the group for support.Still, despite the obvious group intelligence, the monkeys individually didn’t seem particularly smart to Milton. They were relatively dull and placid - and unobservant. I ate lunch for months in full view of dozens of howlers, and not one ever seemed to realize that I was eating, much less that what I was eating might be something they would enjoy, too, she says. You could make noises and slurp and carry on - whatever cognitive processes are required to identify the act of eating, they don’t seem to use them.But spider monkeys did. I saw them all the time when I was studying howlers, says Milton. They’d go roaring by like greased lightning. Spider monkeys are the same size as howlers, and the two animals share parts of each other’s ranges on Barro Colorado. But there the similarities end. Whereas howlers travel through the canopy on all fours, spiders swing along like Tarzan. Unlike the placid howlers, spiders are playful and mischievous. They’re terrible teases, says Milton. And they’re mean little devils. They remind me of people, she confides with a laugh. Although not specifically any of my close friends.Spider monkeys had no trouble recognizing Milton’s lunch. ‘Food!’ they’d shout. ‘Let’s see if we can get it!’ They’d swing down toward you; they’d threaten you. They know what a banana is. They have a keen idea of what a peanut butter sandwich is. You simply cannot eat in front of them.Intrigued, Milton decided she’d add spider monkeys to her observations. She thought it might be interesting to compare how the two species evolved from a common ancestor. But while the comparatively sedate howlers were a researcher’s dream, dealing with the spider monkeys was something else again. They were too fast for me, says Milton. So I hired a young man to work with me. He would run through the forest as fast as he could, following the monkeys, and I would come behind. We communicated by calls. ‘Whooooo!’ Like that. The sound really carries through the forest.When the barnstorming spider monkeys found food, they’d finally screech to a stop, allowing Milton to catch up. They’d just stuff themselves. Then they’d lie around and take naps.Unlike the howlers, Milton discovered, the spider monkeys almost exclusively ate fruit, which often made up 90 percent of their diet. Even when fruit was out of season or in short supply, it constituted over half their food. But ripe fruit is even harder to find than tender leaves. To get enough, the 18 spider monkeys on the island would resort to splitting up and trying their luck on their own. During most of the year the distribution patterns of their foods are such that if they went around in a big group, there wouldn’t be enough at any one site to feed everyone, says Milton. So they’d spend almost the whole day foraging in small subunits or by themselves. Then around twilight they’d begin to call and coalesce, and then they’d spend the night together.As a result of this extended exploring, the spiders’ territory was huge, some 750 acres, ten times that of the howler monkeys. And that’s a conservative estimate, says Milton. Two thousand acres might be right. If the howlers displayed impressive feats of memory and direction by finding young leaves, the spider monkeys’ long-distance forays after fruit were astounding. Within an enormous area they had to remember at least 100 species of fruit and where to find thousands of fruit-bearing trees. They had to remember when each fruit was ripe, how best to approach the site, and how best to return home. If a howler forgot a food source or a travel route, the others were there to take up the slack. The spiders, though, had to fend for themselves.And they had to know how to stay in touch. Howler monkeys tended to be quiet, communicating through subtle clucks and rattles in the throat, except at daybreak, when their eerie howls declared. ...Spider monkeys, on the other hand, were conspicuously noisy. They’d yelp and cry, whinnying like horses, barking like dogs - sometimes for hours at a time. ...And in contrast to the howlers’ community messages, spider monkeys believed in individual expression. Spider monkey vocalizations are generally individualistic. ...All that variety and independence requires lots of training. As a result, infant spider monkeys mature slowly. They are nursed and carried by their mothers for two years, and they continue to associate almost exclusively with her until they’re about three or three and a half years old. ...Why were the two monkeys so dissimilar? Milton wondered about the differences in their diets. Howler monkeys ate mainly leaves, sometimes exclusively leaves, a low-quality source of nutrition. Leaves are plentiful and relatively high in protein, but they’re low in energy-rich carbohydrates. They also consist of some 60 percent indigestible fiber and sometimes contain toxic chemicals. How in the world did howlers get enough energy from this unpromising diet? And why did they stick to it even during seasons when there was plenty of ripe fruit in the forest?Fruits are loaded with easily digested carbohydrates and are relatively low in fiber - they’re high-quality, nutritious food. They mean instant energy. On the other hand, fruits provide little protein. So, Milton wondered, how did spider monkeys get enough protein? And why, when fruits were scarce, didn’t they fill up on leaves, as howlers did? Why did they go to such extremes to find fruits?Milton began finding some answers to these questions in 1977, when she returned to Barro Colorado after completing her doctoral thesis. She soon conducted an experiment measuring how long it took the monkeys to process their food. I needed to look at internal features of the monkeys, she says. I thought that perhaps the structure of their guts or efficiency of their digestion might be influencing their behavior.She trapped howler and spider monkeys, confined them in pens, and fed them food in which she had concealed tiny plastic markers. I used a type of thin plastic material that I cut with very fine manicure scissors into little colored plastic worms, she explains. When the monkeys excreted the remains of their food, out came the markers. Milton could therefore measure the time it took any one meal to pass through a monkey’s digestive tract. The results were dramatic: howlers took 20 hours to digest their food, five times as long as spiders. ...When Milton came upon monkeys that had died in the forest, she took them back to the research station, dissected them, and measured their gastrointestinal tracts. She then confirmed her figures against published material on differential gut measurements in various primates. She found that the colons of howlers were considerably wider and longer than those of spider monkeys. Food had to travel much farther and remained much longer in howler guts, and the monkeys had room for much more bulk. As a result, bacteria had a chance to ferment masses of fibrous leaves in the monkeys’ colons, producing energy-rich fatty acids. Milton eventually found that howlers receive more than 30 percent of their daily energy from such fatty acids.... Spiders were far less efficient at extracting energy from the fiber in their diet - but they didn’t have to be efficient. They ate easily digestible fruits. By moving a steady stream of fruit through their gastrointestinal tracts every day, they obtained all the carbohydrates they needed and some of the protein. The rest came from supplements of young, tender leaves.It was a striking example of evolutionary adaptation. Each monkey’s physiology fit its particular diet. Spider monkeys couldn’t get away with eating a howler diet of mostly leaves. With their smallish guts, they’d never keep enough bulk around long enough for fermentation to provide energy. And howlers wouldn’t manage for long if they used the spider monkey tactic of eating fruit - their slow digestive tracts couldn’t process nearly enough of it. Besides, it took smarts to track down sufficient fruit, and Milton thought it unlikely that the howlers were up to the job. Nor was the howler diet of leaves up to the job of fueling the amount of brainpower necessary. The brain, a big, hungry organ, requires a disproportionate amount of energy, and leaves just don’t provide enough....The more I thought about it, the more it seemed to make sense that if you have a high-energy diet and widely distributed foods, you’re going to need a certain amount of ability to locate those foods. ...A scientist named Daniel Quirling had published extensive statistics about the sizes of primate brains. Spider monkey brains, he had determined, weigh twice those of howlers, 107 grams compared with 50.4. No wonder spiders are smarter....Compared with the howlers, spider monkeys were brighter and more lively. They matured more slowly and had more to learn; they made more ruckus, with a greater variety of vocalizations; they ate widely dispersed, high-energy foods that were harder to find--and their brains were twice as large. Why?As far as Milton was concerned, diet was the key to these discrepancies. Eating fruits fueled the evolution of the spider monkeys’ large brains. Says Milton, It would have been a feedback process in which some slight change in the monkeys’ foraging behavior conferred a benefit, which in turn permitted a modest improvement in the quality of their diet, which led to an excess of energy. Over generations, the monkeys that spent the energy on making their brain slightly bigger and more complex had an evolutionary advantage. Their improved brain allowed for more helpful changes in their behavior, and so on.Milton realized that if such a scenario was correct, similar differences in brain size should show up in other primates with similar differences in diet - monkeys and apes that eat fruits should have larger brains than their leaf-eating counterparts. Sure enough, when Milton checked the literature, she found the pattern held true. For example, of the three great apes, lively, quick chimpanzees, our closest animal relatives, have a bigger brain for their body size than do the slower, more placid gorillas and orangutans. Chimps take some 94 percent of their diet from plants, largely in the form of ripe fruits. Gorillas and orangutans eat 99 percent plant foods, but mainly lower-quality leaves, pith, even bark. Diet had to be the key to their disparate evolution.

ds9.botanik.uni-bonn.de —  ROOT APEX – THE ANTERIOR POLE OF PLANT BODY Root Apices represent the Anterior Pole: Specialized for uptake of nutrients and for neuronal activities. Importantly, new roots are formed endogenously (recapitulation of embryogenesis). Shoot Apices represent the Posterior Pole: Specialized for photosynthesis (which is dispensable in holoparasitic plants like Rafflesia) and for sexual reproduction. The flower is the perfect form of the shoot. Shoots harbor plant organs of excretion, trichomes and hydathodes. Moreover, stomata allow gas exchange. Similarly as sexual organs, also organs of plant excretion and stomata are located at the posterior part of the plant body. Even more, hydathodes seem to function in analogy to kidney (Pilot et al. 2004, Plant Cell 16: 1827-1840). Roots are essential whereas shoots are dispensable: In holoparasitic plants, such as Rafflesia, roots are transformed into haustoria while the green part of the plant is missing completely. Nevertheless, haustoria of Rafflesia form the largest flowers in the plant kingdom which reveals that this unique organism really belongs to plants. AUXIN – PLANT NEUROTRANSMITTER Auxin: Represents a plant-specific neurotransmitter and is transported, in a light- and gravity-dependent manner, preferentially along the anterior-posterior axis of the plant body. Auxin induces the formation of both vascular strands (plant nerves) and roots (which harbour the “serial plant brain”). Roots and Auxin: Root apices represent major sinks for the polar auxin transport. Root apices are extremely sensitive towards externally applied auxin, and lateral root formation is induced by this means. Moreover, auxin rapidly regulates vesicle trafficking and gene expression in roots. Initiation of lateral root primordia is an endogenous process resembling early embryogenesis. In contrast, new shoots and leaves are formed exogenously. CELLULAR END-POLES – PLANT SYNAPSES Plant Synapses: Stable actin-supported adhesive domains (known as end-poles or cross-walls) between adjacent plant cells across which auxin and other chemical signals are transported via actin-based vesicular trafficking pathways. Besides these developmental plant synapses, plants are also capable of forming cell-to-cell junctions with cells of another organisms (plants – fungi – bacteria) corresponding to what is defined as an ‘immunological synapse’. These specialized cell-to-cell adhesion domains involve the plasma membranes of two different organisms opposing each other. Such adhesive domains are also sites of active cell-to-cell transport of molecules and metabolites. VASCULAR STRANDS – PLANT NERVES Vascular Strands: The basic units of the vascular system represent both plant nerves as well as a plant endoskeleton. Leaves contain single strands which combine to form the vascular bundles of the stem, and the vascular cylinder of the root. In roots, the largest portion of the organ is the vascular tissue, and its strands (plant nerves) are supported by numerous cells forming the vascular cylinder. Phloem: Supracellular axon-like ‘channel' interconnecting shoot and root apices. Phloem is specialized for transmission of action-potential-driven electric signals. Axon-like means that it is specialized for the rapid transfer of RNA molecules but does not accomplish ribosome assembly and mRNA translation. Xylem: Non-living and water-filled tubes specialized for transmission of hydraulic signals which are self-transmitting waves induced and driven by changes in hydrostatic pressure. ROOT APICES INTERCONNECTED VIA VASCULAR CYLINDERS – SERIAL NERVOUS SYSTEM OF PLANT Plant Brain: Each root apex harbours a unit of nervous system of plants. The number of root apices in the plant body is high and all brain-units are interconnected via vascular strands (plant nerves) with their polarly-transported auxin (plant neurotransmitter), to form a serial (parallel) nervous system of plants. The computational and informational capacity of this nervous system based on interconnected parallel units is predicted to be higher than that of the diffuse nervous system of lower animals, or the central nervous system of higher animals/humans.

5e.plantphys.net —  A Companion to Plant Physiology, Fifth Edition by Lincoln Taiz and Eduardo Zeiger Topics 1. Plant Cells Topic 1.1, Model Organisms Topic 1.2, The Plant Kingdom Topic 1.3, Flower Structure and the Angiosperm Life Cycle Topic 1.4, Plant Tissue Systems: Dermal, Ground, and Vascular Topic 1.5, The Structures of Chloroplast Glycosylglycerides Topic 1.6, A Model for the Structure of Nuclear Pores Topic 1.7, The Proteins Involved in Nuclear Import and Export Topic 1.8, Protein Signals Used to Sort Proteins to their Destinations Topic 1.9, SNAREs, Rabs, and Coat Proteins Mediate Vesicle Formation, Fission, and Fusion Topic 1.10, ER Exit Sites (ERES) and Golgi Bodies Are Interconnected Topic 1.11, Specialized Vacuoles in Plant Cells Topic 1.12, Actin-Binding Proteins Regulate Microfilament Growth Topic 1.13, Kinesins Are Associated with Other Microtubules and Chromatin Topic 1.14, Chapter One References 2. Genome Organization and Gene Expression Topic 2.1, Recombination Mapping and Gene Cloning Topic 2.2, Transposon Tagging 3. Water and Plant Cells Topic 3.1, Calculating Capillary Rise Topic 3.2, Calculating Half-Times of Diffusion Topic 3.3, Alternative Conventions for Components of Water Potential Topic 3.4, Temperature and Water Potential Topic 3.5, Can Negative Turgor Pressures Exist in Living Cells? Topic 3.6, Measuring Water Potential Topic 3.7, The Matric Potential Topic 3.8, Wilting and Plasmolysis Topic 3.9, Understanding Hydraulic Conductivity Topic 3.10, Chapter Three References 4. Water Balance of Plants Topic 4.1, Irrigation Topic 4.2, Physical Properties of Soils Topic 4.3, Calculating Velocities of Water Movement in the Xylem and in Living Cells Topic 4.4, Leaf Transpiration and Water Vapor Gradients Topic 4.5, Chapter Four References 5. Mineral Nutrition Topic 5.1, Symptoms of Deficiency in Essential Minerals - Wade Berry, UCLA Topic 5.2, Observing Roots below Ground Topic 5.3, Chapter Five References 6. Solute Transport Topic 6.1, Relating the Membrane Potential to the Distribution of Several Ions across the Membrane: The Goldman Equation Topic 6.2, Patch Clamp Studies in Plant Cells Topic 6.3, Chemiosmosis in Action Topic 6.4, Kinetic Analysis of Multiple Transporter Systems Topic 6.5, ABC Transporters in Plants Topic 6.6, Transport Studies with Isolated Vacuoles and Membrane Vesicles Topic 6.7, Chapter Six References 7. Photosynthesis: The Light Reactions Topic 7.1, Principles of Spectrophotometry Topic 7.2, The Distribution of Chlorophylls and Other Photosynthetic Pigments Topic 7.3, Quantum Yield Topic 7.4, Antagonistic Effects of Light on Cytochrome Oxidation Topic 7.5, Structures of Two Bacterial Reaction Centers Topic 7.6, Midpoint Potentials and Redox Reactions Topic 7.7, Oxygen Evolution Topic 7.8, Photosystem I Topic 7.9, ATP Synthase Topic 7.10, Mode of Action of Some Herbicides Topic 7.11, Chlorophyll Biosynthesis Topic 7.12, Chapter Seven References 8. Photosynthesis: The Carbon Reactions Topic 8.1, CO2 Pumps Topic 8.2, How the Calvin–Benson Cycle Was Elucidated Topic 8.3, Rubisco: A Model Enzyme for Studying Structure and Function Topic 8.4, Energy Demands for Photosynthesis in Land Plants Topic 8.5, Rubisco Activase Topic 8.6, Thioredoxins Topic 8.7, Operation of the C2 Oxidative Photosynthetic Carbon Cycle Topic 8.8, Carbon Dioxide: Some Important Physicochemical Properties Topic 8.9, Three Variations of C4 Metabolism Topic 8.10, Single-Cell C4 Photosynthesis Topic 8.11, Photorespiration in CAM plants Topic 8.12, Glossary of Carbohydrate Biochemistry Topic 8.13, Starch Architecture Topic 8.14, Fructans Topic 8.15, Chloroplast Phosphate Translocators Topic 8.16, Chapter Eight References 9. Photosynthesis: Physiological and Ecological Considerations Topic 9.1, Working with Light Topic 9.2, Heat Dissipation from Leaves: The Bowen Ratio Topic 9.3, The Geographic Distributions of C3 and C4 Plants Topic 9.4, Calculating Important Parameters in Leaf Gas Exchange Topic 9.5, Prehistoric Changes in Atmospheric CO2 Topic 9.6, Projected Future Increases in Atmospheric CO2 Topic 9.7, Using Carbon Isotopes to Detect Adulteration in Foods Topic 9.8, Reconstruction of the Expansion of C4 Taxa Topic 9.9, Chapter Nine References 10. Translocation in the Phloem Topic 10.1, Sieve Elements as the Transport Cells between Sources and Sinks - Susan Dunford, University of Cincinnati Topic 10.2, An Additional Mechanism for Blocking Wounded Sieve Elements in the Legume Family - Susan Dunford, University of Cincinnati Topic 10.3, Sampling Phloem Sap - Susan Dunford, University of Cincinnati Topic 10.4, Nitrogen Transport in the Phloem - Susan Dunford, University of Cincinnati Topic 10.5, Monitoring Traffic on the Sugar Freeway: Sugar Transport Rates in the Phloem - Susan Dunford, University of Cincinnati Topic 10.6, Alternative Views of Pressure Gradient in Sieve Elements: Large or Small Gradients? - Susan Dunford, University of Cincinnati Topic 10.7, Experiments on Phloem Loading - Susan Dunford, University of Cincinnati Topic 10.8, Experiments on Phloem Unloading - Susan Dunford, University of Cincinnati Topic 10.9, Allocation in Source Leaves: The Balance between Starch and Sucrose Synthesis - Susan Dunford, University of Cincinnati Topic 10.10, Partitioning: The Role of Sucrose-Metabolizing Enzymes in Sinks Topic 10.11, Possible Mechanisms Linking Sink Demand and Photosynthetic Rate in Starch Storers - Susan Dunford, University of Cincinnati Topic 10.12, Proteins and RNAs: Signal Molecules in the Phloem Topic 10.13, Chapter Ten References - Susan Dunford, University of Cincinnati 11. Respiration and Lipid Metabolism Topic 11.1, Isolation of Mitochondria - Ian M. Møller, Aarhus University, Denmark; Allan G. Rasmusson, Lund University, Sweden Topic 11.2, The Q-Cycle Explains How Complex III Pumps Protons across the Inner Mitochondrial Membrane - Allan G. Rasmusson, Lund University, Sweden; Ian M. Møller, Aarhus University, Denmark Topic 11.3, Multiple Energy Conservation Bypasses in Oxidative Phosphorylation of Plant Mitochondria - Allan G. Rasmusson, Lund University, Sweden; Ian M. Møller, Aarhus University, Denmark Topic 11.4, FoF1-ATP Synthases: The World′s Smallest Rotary Motors - Lincoln Taiz, University of California, Santa Cruz, California, USA Topic 11.5, Transport Into and Out of Plant Mitochondria - Allan G. Rasmusson, Lund University, Sweden; Ian M. Møller, Aarhus University, Denmark Topic 11.6, The Genetic System in Plant Mitochondria Has Several Special Features - Allan G. Rasmusson, Lund University, Sweden; Ian M. Møller, Aarhus University, Denmark Topic 11.7, Does Respiration Reduce Crop Yields? - James N. Siedow, Duke University, North Carolina, USA; Ian M. Møller, Aarhus University, Denmark; Allan G. Rasmusson, Lund University, Sweden Topic 11.8, The Lipid Composition of Membranes Affects the Cell Biology and Physiology of Plants - John Browse, Washington State University Topic 11.9, Utilization of Oil Reserves in Cotyledons - John Browse, Washington State University Topic 11.10, Chapter 11 References 12. Assimilation of Mineral Nutrients Topic 12.1, Development of a Root Nodule Topic 12.2, Measurement of Nitrogen Fixation Topic 12.3, The Synthesis of Methionine Topic 12.4, Oxygenases Topic 12.5, Chapter Twelve References 13. Secondary Metabolites and Plant Defense Topic 13.1, Cutin, Waxes, and Suberin Topic 13.2, Structure of Various Triterpenes Topic 13.3, The Shikimic Acid Pathway Topic 13.4, Detailed Chemical Structure of a Portion of a Lignin Molecule Topic 13.5, Chapter Thirteen References 15. Cell Walls: Structure, Biogenesis, and Expansion Topic 15.1, Plant Cell Walls Play a Major Role in Carbon Flow through Ecosystems Topic 15.2, Terminology for Polysaccharide Chemistry Topic 15.3, Molecular Model for the Synthesis of Cellulose and Other Wall Polysaccharides That Consist of a Disaccharide Repeat Topic 15.4, Matrix Components of the Cell Wall Topic 15.5, The Mechanical Properties of Cell Walls: Studies With Nitella Topic 15.6, Wall Degradation and Plant Defense Topic 15.7, Structure of Biologically Active Oligosaccharins Topic 15.8, Glucanases and Other Hydrolytic Enzymes May Modify the Matrix Topic 15.9, Chapter Fifteen References 16. Growth and Development Topic 16.1, Embryonic Dormancy Topic 16.2, Rice Embryogenesis Topic 16.3, Polarity of Fucus Zygotes Topic 16.4, Azolla Root Development Topic 16.5, Class III HD-Zip Transcription Factors Promote Adaxial Development through a microRNA-Sensitive Mechanism Topic 16.6, During Senescence Photoactive Chlorophyllide Is Converted into a Colorless Chlorophyll Catabolite Topic 16.7, Chapter Sixteen References 17. Phytochrome and Light Control of Plant Development Topic 17.1, Mougeotia: A Chloroplast with a Twist Topic 17.2, Phytochrome and High-Irradiance Responses Topic 17.3, The Origins of Phytochrome as a Bacterial Two-Component Receptor Topic 17.4, Profiling Gene Expression in Plants Topic 17.5, Two-Hybrid Screens and Co-immunoprecipitation Topic 17.6, Phytochrome Effects on Ion Fluxes Topic 17.7, Microarray Analysis of Shade Avoidance Topic 17.8, Chapter Seventeen References 18. Blue-Light Responses: Morphogenesis and Stomatal Movements Topic 18.1, Blue-Light Sensing and Light Gradients Topic 18.2, Guard Cell Osmoregulation and a Blue Light-Activated Metabolic Switch Topic 18.3, The Coleoptile Chloroplast Topic 18.4, Phytochrome-Mediated Responses in Stomata Topic 18.5, Chapter Eighteen References 20. Gibberellins: Regulators of Plant Height and Seed Germination Topic 20.1, Structures of Some Important Gibberellins and Their Precursors, Derivatives, and Inhibitors of Gibberellin Biosynthesis - Valerie Sponsel, Biology Department, University of Texas, San Antonio, Texas, USA Topic 20.2, Commercial Uses of Gibberellins - Valerie Sponsel, Biology Department, University of Texas, San Antonio, TX, USA Topic 20.3, Gibberellin Biosynthesis - Valerie Sponsel, Biology Department, University of Texas, San Antonio, TX, USA Topic 20.4, Gas Chromatography—Mass Spectrometry of Gibberellins - Valerie Sponsel, Biology Department, University of Texas, San Antonio, TX, USA Topic 20.5, Environmental Control of Gibberellin Biosynthesis - Valerie Sponsel, Biology Department, University of Texas, San Antonio, TX, USA Topic 20.6, Auxin Can Regulate Gibberellin Biosynthesis - Jocelyn A. Ozga and Dennis M. Reinecke, Plant BioSystems Group, Department of Agricultural, Food, and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada T6G 2P5 Topic 20.7, Negative Regulators of GA Response - Valerie Sponsel, Biology Department, University of Texas, San Antonio, TX, USA Topic 20.8, Effects of GAs on Flowering - Valerie Sponsel, Biology Department, University of Texas, San Antonio, TX, USA Topic 20.9, DELLA Proteins as Integrators of Multiple Signals - Stephen G. Thomas, Rothamsted Research, Harpenden, United Kingdom Topic 20.10, Chapter Twenty References 21. Cytokinins: Regulators of Cell Division Topic 21.1, Cultured Cells Can Acquire the Ability to Synthesize Cytokinins Topic 21.2, Structures of Some Naturally Occurring Cytokinins Topic 21.3, Various Methods Are Used to Detect and Identify Cytokinins Topic 21.4, The Biologically Active Form of Cytokinin Is the Free Base Topic 21.5, Cytokinins Are Also Present in Some tRNAs in Animal and Plant Cells Topic 21.6, The Structures of Opines Topic 21.7, The Ti Plasmid and Plant Genetic Engineering Topic 21.8, Phylogenetic Tree of IPT genes Topic 21.9, A Root-Derived Hormone, Strigolactone, Is Involved in the Suppression of Branching in Shoots Topic 21.10, Cytokinin Can Promote Light-Mediated Development Topic 21.11, Cytokinins Promote Cell Expansion and Greening in Cotyledons Topic 21.12, Cytokinins Interact with Elements of the Circadian Clock Topic 21.13, Chapter Twenty-One References 22. Ethylene: The Gaseous Hormone Topic 22.1, Ethylene in the Environment Arises Biotically and Abiotically Topic 22.2, Ethylene Readily Undergoes Oxidation Topic 22.3, Ethylene Can Be Measured by Gas Chromatography Topic 22.4, Cloning of the Gene That Encodes ACC Synthase Topic 22.5, Cloning of the Gene That Encodes ACC Oxidase Topic 22.6, Ethylene Binding to ETR1 and Seedling Response to Ethylene Topic 22.7, Conservation of Ethylene Signaling Components in Other Plant Species Topic 22.8, ACC Synthase Gene Expression and Biotechnology Topic 22.9, The hookless Mutation Alters the Pattern of Auxin Gene Expression Topic 22.10, Ethylene Inhibits the Formation of Nitrogen-Fixing Root Nodules in Legumes Topic 22.11, Ethylene Biosynthesis Can Be Blocked with Anti-Sense DNA Topic 22.12, Abscission and the Dawn of Agriculture Topic 22.13, Specific Inhibitors of Ethylene Biosynthesis Are Used Commercially to Preserve Cut Flowers Topic 22.14, Chapter Twenty-Two References 23. Abscisic Acid: A Seed Maturation and Stress-Response Hormone Topic 23.1, The Structure Of Lunularic Acid from Liverworts Topic 23.2, ABA May Be an Ancient Stress Signal Topic 23.3, Structural Requirements for Biological Activity of Abscisic Acid Topic 23.4, The Bioassay of ABA Topic 23.5, Evidence for Both Extracellular and Intracellular ABA Receptors Topic 23.6, The Existence of G Protein-Coupled ABA Receptors Is Still Unresolved Topic 23.7, The Yeast Two-Hybrid System Topic 23.8, Yellow Cameleon: A Noninvasive Tool for Measuring Intracellular Calcium Topic 23.9, Phosphatidic Acid May Stimulate Sphingosine-1-Phosphate Production Topic 23.10, The ABA Signal Transduction Pathway Includes Several Protein Kinases Topic 23.11, The ERA1 and ABH Genes Code for Negative Regulators of the The ABA Response Topic 23.12, Promoter Elements That Regulate ABA Induction of Gene Expression Topic 23.13, Regulatory Proteins Implicated in ABA-Stimulated Gene Transcription Topic 23.14, ABA Gene Expression Can Also Be Regulated by mRNA Processing and Stability Topic 23.15, ABA May Play a Role in Plant Pathogen Responses Topic 23.16, Proteins Required for Desiccation Tolerance Topic 23.17, The Types of Coat-Imposed Seed Dormancy Topic 23.18, Types of Seed Dormancy and the Roles of Environmental Factors Topic 23.19, The Longevity of Seeds Topic 23.20, Genetic Mapping Of Dormancy: Quantitative Trait Locus (QTL) Scoring of Vegetative Dormancy Combined with a Candidate Gene Approach Topic 23.21, ABA-Induced Senescence and Ethylene Topic 23.22, Chapter Twenty-Three References 25. The Control of Flowering Topic 25.1, Contrasting the Characteristics of Juvenile and Adult Phases of English Ivy (Hedera helix) and Maize (Zea mays) Topic 25.2, Regulation of Juvenility by the TEOPOD (TP) Genes in Maize Topic 25.3, Flowering of Juvenile Meristems Grafted to Adult Plants Topic 25.4, Characteristics of the Phase-Shifting Response in Circadian Rhythms Topic 25.5, Support for the Role of Blue-Light Regulation of Circadian Rhythms Topic 25.6, Genes That Control Flowering Time Topic 25.7, Regulation of Flowering in Canterbury Bells by Both Photoperiod and Vernalization Topic 25.8, The Self-Propagating Nature of the Floral Stimulus Topic 25.9, Examples of Floral Induction by Gibberellins in Plants with Different Environmental Requirements for Flowering Topic 25.10, The Effects of Two Different Gibberellins on Flowering (Spike Length) and Elongation (Stem Length) Topic 25.11, The Contrasting Effects of Phytochromes A and B on Flowering Topic 25.12, A Gene That Regulates the Floral Stimulus in Maize Topic 25.13, Chapter Twenty-Five References 26. Responses and Adaptations to Abiotic Stress Topic 26.1, Stomatal Conductance and Yields of Irrigated Crops Topic 26.2, Membrane Lipids and Low Temperatures Topic 26.3, Ice Formation in Higher-Plant Cells Topic 26.4, Water-Deficit-Regulated ABA Signaling and Stomatal Closure Topic 26.5, Genetic and Physiological Adaptations Required for Zinc Hyperaccumulation Topic 26.6, Cellular and Whole Plant Responses to Salinity Stress Topic 26.7, Signaling during Cold Acclimation Regulates Genes That Are Expressed in Response to Low Temperature and Enhances Freezing Tolerance Topic 26.8, Chapter Twenty-Six References