To shard blockchain without sharding consensus, add intermediary level, a validator manager or government . The voting (coin-vote or people-vote) is for government and not for block producers directly. The governments then delegate authority to one block producer per shard.
Simple commit-reveal scheme at the core, such as many RNG systems use. Difference is it relies on very large number of participants that submit "entropy". Avoids issue of choose-to-not-reveal attacks & such, by not simply combining revealed "entropy" into a random number, but rather letting revealed entropy act as vote to select number between 0 and number of participants. By Poisson distribution, known that for given number of participants, the number that receives most votes (assuming random votes) will reach a specific number of votes (such as 13 for 8 billion participants).
Participants cannot know what number they submit. I.e., "entropy" they submit has to "mutate" after they have submitted it. Use result of previous round to change value of each submitted number. For example, hash each contribution with result of previous round + address of submitter.
Has to be "bootstrapped" with secure initial seed. Attack on initialization is discoverable (results not by Poisson distribution). If attacked, initialize again. Repeat until securely initialized.
# Reverse osmosis effect in narrow tubes concentrates urine in the kidney
Contrary to normal ("forward") osmosis, reverse osmosis moves water against the osmolarity gradient, from the salt water side to the fresh water side. It allows the production of fresh water from salt water, and is the most widely used desalination method worldwide. Reverse osmosis is normally pressure-based, but, a different type of reverse osmosis takes place in narrow tubes (micrometer scale) that also moves water in the direction opposite to normal osmosis, and therefore allows the production of fresh water. Such an effect is the basis of how the kidney concentrates urine, and it takes place in the thin segment of the nephron (it is why the nephron has evolved a narrow segment. )
In the kidney, the narrow tube effect is amplified by pressure, and the kidney adjusts how much it wants to concentrate the filtrate by adjusting the glomerular filtration pressure. To do this, it has evolved the tubuloglomerular feedback system in the juxtaglomerular apparatus. The role of tubuloglomerular feedback is simply to regulate the strength of the reverse osmosis effect in the thin segment, and it acts both locally via renin and systemically via angiotensin to achieve sufficient filtration pressure. This allows the body to prevent dehydration.
The kidney thus concentrates urine by pressure, although the pressure itself is not the basis of the effect, it only amplifies the effect that is inherent to narrow tubes.
# The role of adsorbed water in the mechanism of osmosis
It was discovered in 2009 that the driving force for osmosis is the thin layer of adsorbed water that forms at hydrophilic surfaces. This adsorbed phase of water has the unusual (and unpredicted) property of being charge polarized, it releases protons into the surrounding water that gets positively charged, and itself gains a negative charge from the surplus of hydroxide ions it is left with. The force behind this charge polarization effect is analogous to the force in semiconductor junctions: diffusion, from thermal energy. Water in the adsorbed phase (that is a semi-solid phase that is halfway between liquid and solid phase) auto-ionizes just like liquid water, but contrary to water in the liquid phase the hydroxide ions are locked into the semi-solid mass that is anchored to the hydrophilic surface. The more mobile hydrogen ion will diffuse outwards to a larger extent than the hydroxide ion, causing the charge separation effect.
Osmosis happens when there is an asymmetry between the thickness of the adsorbate on either side of a membrane. The asymmetry will cause protons to "even out their concentration" around the combined negative mass of the adsorbates on either side, so that the charge distribution is balanced out. The relative surplus and deficit of protons that results, will cause hydroxide ions on the exosmotic side (where water is moving from) to break down into dioxide, water and electrons, and the electrons will transfer over to the endosmotic side where there is a surplus of protons, and combine with the protons and dioxide to form dihydrogen monoxide, water. Water itself does not physically "move", it is broken down and built up on either side of the membrane. Only electrons and protons move during osmosis. The effect is analogous to what takes place in an acid-base battery.
Salt impairs the formation of the adsorbed phase in the same way it impairs the solid phase by freezing point depression (a colligative property), and an increase in osmolarity on one side will decrease the amount of adsorbate at the membrane on that side, causing the effect of proton equilibration and the subsequent breakdown of hydroxide ions on the hypoosmotic side of the membrane. Pressure, acts in an opposite way to increase the thickness of the adsorbate, and therefore generates an osmotic transfer of water in the reverse direction to osmolarity-based osmosis, away from the pressure.
In narrow tubes, the proximity of the adsorbate around the circumference of the tube and across the diameter causes an increase in the net positive charge of the lumen of the tube, and this effect will be yet another factor in how the protons even out their concentration (charge wise) across both sides of the membrane of the tube. This provides a method for reverse osmosis that can operate at very low pressures, such as that within the filtration system of the kidney. Since pressure increases the amount of adsorbate, it also increases the repulsion effect in the lumen of narrow tubes, and this allows the kidney to regulate the strength of the urine concentration mechanism by regulating the filtration pressure.
# The loop of Henle recirculates dioxide, the cathode in osmosis
The glomerular filtration tubular reabsorption pattern is physiologically complicated, and the peculiar and intricate loop design of the nephron has motivated a physiological model that explained why such as loop had been selected for, evolutionarily. This motivated the theory that the kidney operated by forward osmosis (osmolarity-based) and generated an osmolarity gradient using a counter-current multiplication mechanism, and that the loop of Henle had evolved to facilitate this process. The true reason for the loop of Henle is much more directly tied to the mechanism of osmosis: it recirculates the dioxide that is required for the cathode reaction in osmosis, so that the reverse osmosis process in the thin segment can reabsorb more water than would otherwise be possible with a single-pass of the dioxide.
The recirculation of dioxide is complicated and it explains the complicated patterns of reabsorbtion in the kidney. Dioxide is relased into the nephron in the thin segment (thin descending limb) when water is reabsorbed by reverse osmosis (and transported out of the kidney via the ascending vasa recta. ) This dioxide has to be returned into the medulla and the blood stream, or it will be extreted in the urine. To reabsorb the dioxide, the kidney uses osmosis all over again, and moves water back into the ascending thin limb of the loop of Henle. This seemingly counterproductive arrangement, where there is no net osmotic transfer of water, has evolved to faciliate the non-osmotic reabsorbtion of water from the collecting duct system. The reverse osmosis in the thin descending limb dehydrates the medulla, and favours the diffusion of water from the collecting duct tree and concentrates the urine before it leaves through the papilla. The water reabsorbed from the collecting duct, is in a 1:1 relationship with the water that is osmotically transferred into the thin ascending limb. The water that loops around from the collecting duct to the ascending thin limb and back again, faciliates the recirculation of dioxide via the vasa recta (that moves in the direction opposite to the loop of Henle. )
# Tubuloglomerular feedback is subordinated vasopressin, and operates reflexively to decisions by the hypothalamus
Tubuloglomerular feedback responds to vasopressin, and vasopressin is ultimately the control mechanism for urine concentration, thereby subordinating the kidney under the hypophysis and the brain. The role of vasopressin is to increase the resistance in the collecting duct tree, by contracting fibroblast-like cells in the kidney medulla, and also to increase water permeability of the collecting duct epithelium by aquaporin channels. The tubuloglomerular autoregulatory system responds to an increase in water reabsorbtion from the collecting duct, by sensing a decrease in filtrate osmolarity at the macula densa region of the thick ascending limb, and upregulates the reverse osmosis mechanism in the thin descending limb of the loop of Henle by increasing the glomerular filtration pressure through renin and angiotensin. Or, rather, it senses only osmolarity increase (concentrating urine more than what is required by vasopressins effect), and release of renin is the default and it gets downregulated whenever macula densa senses that the urine is concentrated more than it should be.
# Reverse osmosis effect in narrow tubes concentrates urine in the kidney
Contrary to normal osmosis, reverse osmosis moves water against the osmolarity gradient, from the salt water side to the fresh water side. It allows the production of fresh water from salt water, and is the most widely used desalination method worldwide. Reverse osmosis is normally pressure-based, but, a different type of reverse osmosis takes place in narrow tubes (micrometer scale) that also moves water in the direction opposite to normal osmosis, and therefore allows the production of fresh water. Such an effect is the basis of how the kidney concentrates urine, and it takes place in the thin segment of the nephron (it is why the nephron has evolved a narrow segment. )
In the kidney, the narrow tube effect is amplified by pressure, and the kidney adjusts how much it wants to concentrate the filtrate by adjusting the glomerular filtration pressure. To do this, it has evolved the tuberoglomerular feedback system in the juxtaglomerular apparatus. The role of tuberoglomerular feedback is simply to regulate the strength of the reverse osmosis effect in the thin segment, and it acts both locally via renin and systemically via angiotensin to achieve sufficient filtration pressure. This allows the body to prevent dehydration.
The kidney thus concentrates urine by pressure, although the pressure itself is not the basis of the effect, it only amplifies the effect that is inherent to narrow tubes.
# The role of adsorbed water in the mechanism of osmosis
It was discovered in 2009 that the driving force for osmosis is the thin layer of adsorbed water that forms at hydrophilic surfaces. This adsorbed phase of water has the unusual (and unpredicted) property of being charge polarized, it releases protons into the surrounding water that gets positively charged, and itself gains a negative charge from the surplus of hydroxide ions it is left with. The force behind this charge polarization effect is analogous to the force in semiconductor junctions: diffusion, from thermal energy. Water in the adsorbed phase (that is a semi-solid phase that is halfway between liquid and solid phase) auto-ionizes just like liquid water, but contrary to water in the liquid phase the hydroxide ions are locked into the semi-solid mass that is anchored to the hydrophilic surface. The more mobile hydrogen ion will diffuse outwards to a larger extent than the hydroxide ion, causing the charge separation effect.
Osmosis happens when there is an asymmetry between the thickness of the adsorbate on either side of a membrane. The asymmetry will cause protons to "even out their concentration" around the combined negative mass of the adsorbates on either side, so that the charge distribution is balanced out. The relative surplus and deficit of protons that results, will cause hydroxide ions on the exosmotic side (where water is moving from) to break down into dioxide, water and electrons, and the electrons will transfer over to the endosmotic side where there is a surplus of protons, and combine with the protons and dioxide to form dihydrogen monoxide, water. Water itself does not physically "move", it is broken down and built up on either side of the membrane. Only electrons and protons move during osmosis. The effect is analogous to what takes place in an acid-base battery.
Salt impairs the formation of the adsorbed phase in the same way it impairs the solid phase (a colligative property), and an increase in osmolarity on one side will decrease the adsorbate at the membrane on that side, causing the effect of proton equilibration and the subsequent breakdown of hydroxide ions on the hypoosmotic side of the membrane. Pressure, acts in an opposite way to increase the thickness of the adsorbate, and therefore generates an osmotic transfer of water in the reverse direction to osmolarity-based osmosis.
In narrow tubes, the proximity of the adsorbate around the circumference of the tube causes an increase in the net positive charge of the lumen of the tube, and this effect will be yet another factor in how the protons even out their concentration (charge wise) across both sides of the membrane of the tube. This provides a method for reverse osmosis that can operate at very low pressures, such as that within the filtration system of the kidney.
# Liquids that can auto-ionize show a p-n junction effect when adsorbed to surfaces
ABSTRACT: When the adsorbed phase of a liquid auto-ionizes by transfer of a hydrogen ion, the conjugate anion is locked into the adsorbed phase, while the hydrogen ion is free to move by diffusion. The diffusion current of the protons is opposed by a drift current within the electric field that forms as the adsorbate loses protons to the liquid and gets negatively charged. The equilibrium between these currents is a separation of charges into a negatively charged adsorbate with a positively charged layer of liquid on top of it. This effect is analogous to the charge polarization seen at the p-n junction in semiconductors like a diode or transistor.
# Liquids that can auto-ionize show a p-n junction effect when adsorbed to surfaces
Consider individual molecules in a liquid such as methanol or water. At surfaces these molecules can bind to, each molecule that anchors to the surface can serve as an anchor for further molecules, and so forth. With this effect, multiple layers of immobile molecules can form at the surface. The molecules will also bond sideways within each layer, and should orient themselves in whatever way fits best. The organization that forms should be an intermediary between the solid phase of the substance, and the liquid phase.
If the liquid can auto-ionize by transfer of a hydrogen ion, the hydrogen ion will be free to move while the conjugate anion is locked into the adsorbed phase. As the hydrogen ions diffuse outwards, an electric field strength will increase between the then negatively charged adsorbed phase, and the surrounding protonated liquid. The equilibrium is a separation of charges into a positively charged layer of liquid phase on top of the negatively charged adsorbed phase. Because the charges are physically separated, the probability of recombination of the ions is reduced, and the result is an increase in the number of ionized molecules.
# The auto-ionization of absorbed water at hydrophilic surfaces
Consider individual water molecules, that are hydrogen bonded to a hydrophilic surface (i.e., a surface that can hydrogen bond to water molecules. ) These molecules will physically anchor to the surfaces, and can also hydrogen bond to other water molecules, providing an anchor to them as well. With this effect, multiple layers of immobile water can form at the hydrophilic surface. The water will also hydrogen bond sideways within each layer, and should orient themselves in whatever way fits best. The organization that forms should be an intermediary between the solid phase of water - ice - and the liquid phase, and probably more towards the solid phase. Since this intermediary is partially liquid, hydrogen bonds in it will continuously break and reform. Every time a hydrogen bond is broken, there is a probability of transferring a hydrogen ion from one water molecule to the other. These hydrogen ions will be mobile relative to the adsorbed water that is immobile, and can gradually diffuse away, while the hydroxide ions remain locked into the adsorbed phase. As the hydrogen ions diffuse outwards, an electric field strength will increase between the then negatively charged adsorbed water, and the surrounding hydronium ions. The equilibrium is a separation of charges into a positively charged layer of liquid water on top of the negatively charged adsorbed phase. Because the charges are physically separated, the probability of recombination of the ions to water is reduced, and the result is an increase in the number of ionized water molecules.
# The auto-ionization in microscopic ice layer at hydrophilic surfaces
ABSTRACT: Water at hydrophilic surfaces forms an up to 0.5 mm thick layer of ice, anchored to the surface by hydrogen bonds. The auto-ionization of this ice behaves differently from liquid water, because of an inequality between the ionic constituents. There is a higher degree of ionization than in liquid water, and the ionic constituents are also physically compartmentalized from one another. This physical compartmentalization results from an inequality in how mobile the ions are. The hydrogen ions are free to move, but the hydroxide ions are locked with hydrogen bonds inside the molecular lattice of the solid phase. The hydrogen ions ability to diffuse allows them to escape outwards into the surrounding water, and the negative charge that builds up in the ice keeps the ejected hydrogen ions close to it. The result is that the ions and their charges are physically polarized into a negatively charged ice layer, and a positively charged layer of water on top of it. This physical compartmentalization prevents reassociation of the ions into water, and contributes to the high degree of ionization seen in the ice. The different constraints for reassociation also provide a force to grow the ice. Each new one-atom thick molecular sheet is nucleated on top of the ice from the positively charged surrounding water. Like with the auto-ionization of liquid water, the ionization increases with temperature, including heating by infrared radiation. The negative charge of the ice is stabilized by hydrostatic pressure, and the ice increases in thickness as pressure increases.
# Is exclusion zone water simply "ionized ice ?
ABSTRACT: Water at hydrophilic surface forms a phase that excludes particles. This phase has been proven to release hydrogen ions into the surrounding water, leaving a negatively charged, hydroxide-rich, solid phase where particles are excluded, and positively charged, hydronium-rich, liquid water around it. This charge polarization might be comparable to the p-n junction in a diode. At the p-n junction, electrons transfer from the negatively doped (n-type) silicon into the positively doped (p-type) silicon, as a result of diffusion into the electrically conductive p-type silicon. The electric field that forms pulls the electrons back towards the n-type silicon, in a drift current . The equilibrium between the diffusion current and drift current is a charge polarized double layer at the p-n junction.
# Introduction
In 1947, Bell Laboratories demonstrated the first working transistor. The physical basis of the transistor is the charge polarized double layer that forms at the p-n junction. Thanks to this charge polarization effect, transistors can be turned on and off by a tiny electrical voltage. The laws of physics that support the charge polarization at the p-n junction, formed the basis of the computer revolution, and the modern world. What if similar physical principles also explain the charge polarization effect seen when water contacts hydrophilic surfaces?
Normal ice will exclude particles. Hydrophilic surfaces allow water to hydrogen bond to the surface, and can support the formation of a single molecular layer of ice. This initial layer, anchored to the hydrophilic surface, in turn allows water in the liquid phase to hydrogen bond to it, and supports another one-atom thick layer of ice. This effect is why hydrophilic materials support ice formation.
The exclusion zone phenomena occurs at temperatures far above the melting point of ice. At these temperatures, hydrogen ions in the ice will have high kinetic energy, and diffuse out into the surrounding liquid water (that is conductive to the diffusion of hydrogen ions. ) Like in a transistor, an electric field will form, and it pulls the hydrogen ions back towards the ice. The equilibrium is a charge polarized double-layer.
This ionization prevents the ice from growing larger than a few hundred micrometers, because of the strong negative charge in the ice.
# Prior work
The charge polarization effect in the interfacial water phase has been discovered and documented by Gerald Pollack and colleagues, and many effects of it have been discovered such as that it is the cause of osmosis. The charge polarization has been theorized to result from a compression of the normal solid phase of ice, each molecular sheet is free to move relative to the others, like a liquid made up of individual one-atom thick layers of ice. Hydrogen ions are ejected because of the compression. The phase is stable because each atomic sheet is shifted slightly, so that oxygen atoms face hydrogen atoms.
This liquid-solid phase of water, that Gerald Pollack named the fourth phase of water , could very well be what exclusion zone water looks like at the molecular level. The compression is one explanation of why hydrogen ions are ejected from the phase. But, diffusion and drift of hydrogen ions is also a possible explanation.
# Ice as a p-type material relative to liquid water
Ice, at temperatures above the freezing point where hydrogen ions will tend to diffuse out of the ice, can be defined as a p-type material relative to the bulk water (that is n-type ). The reason is that the hydroxide ions within the ice are locked in place much more strongly than the hydrogen ions. When a hydrogen ion is able to escape by diffusion, the hydroxide ion remains locked in place. This can be contrasted to the auto-ionization of water where the OH- and H3O+ will sort of dance along with each other through the water, and the drift current will dance along the diffusion current . The ice therefore can only release hydrogen ions (or holes if using the same terminology as with semiconductors), while electrons can be thought of as moving from the bulk water into the ice (again borrowing the terminology used in semiconductors, where only one charge carrier moves but the other is conceptualized as moving in the opposite direction. ) Thus, the ice is p-type relative to the bulk water, the bulk water releases electrons, and the ice releases holes .
This model for the charge polarized double layer in interfacial water is thus truly analogous to a p-n junction, a junction between a positive-type and negative-type material where exchange of charge carriers occurs.
# The p-n junction or the fourth phase of water?
Many effects that have been discovered to be caused by the interfacial water phase, such as osmosis, rely on the charge polarization effect. As such, they could also be explained by a p-n junction mechanism for the charge polarization.
Journal of Clinical Investigation published in 1940 that perfusing a dead heart with 400 mm hg generates current from endocardium to epicardium of one half millivolt. https://www.jci.org/articles/view/101181/pdf
>_"With a pressure of 40 cm. of mercury an amount of current in excess of one half millivolt was produced. "_
>_"These facts are significant in that they indicate that the T-wave is a product of cardiac contraction and contradict the current explanation based on the theory of repolarization. "_
This supports that the heart is an electrical generator that relies on pressure to generate osmotic electrical currents.
I have proven similar things in other physiological systems, most importantly the loop of Henle.
# Reference
MILLER, J. R. AND R. F. DENT. A new hypothesis of the production of the T wave in the electrocardiogram based on electro-kinetic phenomena. J. Clin. Investigation 19: 783, 1940.
Found via Katz, Louis N. (1947). THE GENESIS OF THE ELECTROCARDIOGRAM. Physiological Reviews, 27(3), 398 435. doi:10.1152/physrev.1947.27.3.398
The atmosphere is packed with hydrogen ions, as has been suggested by Gerald Pollack in his 2013 book. This fact has not been widely known, it makes sense if one studies Pollacks 2009 experiment that proves the actual mechanism behind osmosis. This means that the atmosphere has the conditions to act as both poles of a battery, it can store electrons, in water where the oxygen stores 2 extra electrons, and it can release electrons, in O2. This chemical balance is the basis of many mechanisms in biology that have yet to be understood (I have documented many. )
The top capacities in Wyrdenclyffe that were assumed to act by capacitance, storing electricity, actually act by providing the surface area for electrochemical reactions that "store" the electricity in the same way a battery does. They are not capacitor plates, they are electrochemical cells.
This means that they have a much greater "storage" potential than assumed, since they are not what store the charges, the atmosphere itself is.
The chemical reactions are simple 4 H+ + 4 e- + O2 <=> 2 H2O, reversible. It can accept alternating current easily. It also accepts direct current, as you see here, https://www.youtube.com/watch?v=2rVdEhyMR6A.
The triphosphate tail of ATP binds into the "p-loop motif" at the ATP protein binding site on protein. The bonds here are hydrogen bonds, assumed to use the (deprotonated) hydroxyl group on ATP as the bond acceptor.
I think it is actually the bond donator. But this requires that it is fully protonated.
The hydrogen donor in a hydrogen bond is electron withdrawing , whereas the acceptor is "electron donating".
The following model resolves why a negatively charged molecule like ATP could be "electron withdrawing", like Gilbert Ling said.
I want ATP to be fully protonated so that it can store the cathode for the electrical circuits of the cell, H+, after it is displaced from the surface phase (H3O2-)n by K+, because K+ is able to bind more strongly. This increases the distance from the anode to the cathode reaction, it places a "wire" between them. It extends the electrical circuit.
Compared to a protonated group, deprotonated groups are clearly less negatively charged. Because they can't hold onto a proton, while the protonated can. The acceptor in a hydrogen bond, should favourably be the atom with the most negative charge. This is a good start. But, the unprotonated lacks a proton, so it is "relatively" more charged. But what if that proton was re-introduced again?
While the negative charge of the deprotonated hydroxyl groups in ATP might not be enough to hold onto a proton, the added charge of the hydrogen bond acceptors in the protein binding site & both acting on the proton together, might.
Like, a "lock in key" fit for.... a proton. With it, ATP outside protein binding site is _not_ protonated. It only stores protons when it is bound, ensuring their release when it is hydrolysed. And because it stores protons, it also becomes "electron withdrawing", via the hydrogen bonds, of which there are many.
So, the p-loop/ATP complex is acting like a base, using a lock-in-key fit for... protons. And it is why ATP is electron withdrawing.
The loop of Henle has evolved because osmosis consumes and produces dioxygen, O2, and the looped thin segment allows the O2 produced within the thin descending limb during exosmosis, to recirculate out of the thin ascending limb and into the vasa recta, that flows in the opposite direction to the filtrate to return the O2 to the ascending vasa recta. The pump that generates osmotic transfer of water, is the phase that water forms as it is forced into a solid phase when it contacts surfaces. This surface phase is charge polarized, because the hydrogen ions that separate the lattice sheets in the ice phase of water have been squeezed out , to make it more dense than water (the only way a phase change from pressure against surfaces is favourable), and the excluded hydrogen ions protonate water on top of this solid phase. Traditional osmosis is a result of asymmetry in this phase on either side of a membrane, from that the solid phase of water is impaired by solutes. But that is not the only way this pump can generate osmosis. In a narrow tube, the positively charged surface of this phase will repel across the diameter of the tube, pushing protons across the tube wall, causing the negatively charged (H3O2-)n phase to break down into electrons, that transfer across the wall as well, and O2, while the protons and electrons combine with O2 on the outside of the tube to form water.
This osmosis effect in narrow tubes is the physiological basis for the kidney. It removes water from the filtrate (via the ascending vasa recta that drains into the interlobular artery), and dehydrates the medulla. The reason the narrow tube has formed a loop, is that a straight tube that drained into the papilla would also lose all the O2 that was produced in the osmotic pump mechanism. But a tube that loops, could return the O2 to be used again, by reversing the osmosis. The kidney evolved the loop of Henle to do exactly that, and it has oriented the vasa recta in the opposite flow direction specifically to recirculate the O2.
The recirculation of O2, is in a 1:2 relationship with another recirculation system, the H2O that is transferred osmotically to consume O2 at the thin ascending limb. This water recirculates from the collecting duct, and into the thin ascending limb. It dilutes the filtrate as it travels from the bend of the loop of Henle and into the collecting duct, but is then reabsorbed, leaving the filtrate isotonic with what it was at the bend of the loop of Henle. It is there only to maintain the recirculation of the O2. The result is the same as if a straight tube that drained into the papilla received infinite O2.
To support the endosmosis at the thin ascending limb that transfers the O2 in the loop of Henle back into the vasa recta, this segment has evolved a lumen diameter that is gradually increasing, all the way from the bend of the loop of Henle up to the thick ascending limb. Any surplus water, besides that necessary to recirculate the O2, is prevented from entering the medulla, by the low blood supply to the medulla that the kidney evolved to avoid adding any water after the desalination takes place at the thin descending limb.
The kidney is able to increase or decrease the desalination effect at the thin descending limb, by regulating filtration pressure. Less pressure means less water is forced into the surface phase , and a weaker repelling force across the lumen. The kidney has evolved so that the filtration pressure is strongest in the tubes that supply the largest surface area, the juxtamedullary nephrons with long loops that reach the inner medulla. It supplies these glomeruli with more proximal branches from the interlobular artery.
The recirculation of water is regulated by the resistance to flow in the collecting duct tree, and, the permeability to water in the collecting duct epithelia. The hormone vasopressin, secreted by the posterior lobe of the pituitary gland, regulates both of these. It contracts fibroblasts in the medulla, shrinking the diameter of the collecting duct, and, it upregulates aquaporin channels in the epithelial cells.
Kidney function has to be maintained even as systemic pressure, cardiac output, changes with different activities, such as at rest or during physically demanding activity. It has evolved a reflex to do exactly this, tubuloglomerular feedback at the juxtaglomerular apparatus. It is able to maintain filtration pressure even as systemic pressure changes. This ensures that the desalination mechanism at the thin descending limb, is proportional to the recirculation of water, i.e., that the kidney does what the hypothalamus tells it to do (via vasopressin, the antidiuretic hormone) regardless of if the body is at rest or not.
"The purpose of the counter-current system in the loop of Henle is to reabsorb the O2 that is produced in the thin descending limb during the osmotic reabsorption of water there, that is how and where the kidney desalinates water and reabsorbs it into the renal vein. Without the loop, the O2 trapped in the nephron would just pass straight out into the urine, allowing only a one-time use of the osmosis cathode O2. If the body absorbs 22 mol O2 per day, and 1/5th of that passes into the kidney, there is only 4.4 mol O2 in the kidney, and if all of it were used for the desalination mechanism, without recirculation, it could only reabsorb 2*4.4 mol water, equal to 8.8/55.5 = 15 dL, far from the 10 L/d of water that is removed with the thin descending limb of the loop of Henle. The counter-current loop, and the vasa recta flowing in the opposite direction, allows the O2 to recirculate, and using 4.4 mol O2 as an example again, recirculating 63 times provides the osmotic cathode to reabsorb 10 liters of water per day, 63*8.8 mol / 55.5 mol/L = 10 L. "
The pressure from glomerular filtration pushing water into the thin descending limb, and against the epithelium in it, is generating a charge polarized phase of water against the surface, that is positively charged towards the lumen, causing it to repel itself, and pump protons and electrons across the thin epithelium (while producing dioxygen), that recombine with dioxygen in the ascending vasa recta to produce water, that is transported out into the interlobular vein. This makes the filtrate that passes into the medulla and through the bend of the loop of Henle hypertonic, allowing water to transport from the collecting duct into the thin ascending limb, osmotically, aided by the continuous lumen diameter increase in the thin ascending segment, and the dioxygen produced in the thin descending limb. The generation of an "osmotic" removal of water from the thin descending limb, generated by "diametric repulsion" on the surface phase of water, is the physiological basis of the kidney. It is maintained by the juxtaglomerular apparatus, where macula densa cells at the distal convoluted tubule sense the osmolarity of the filtrate, the balance between water removal at the thin descending limb, and water transfer from the collecting duct into the thin ascending limb, and increase glomerular filtration pressure by release of renin that constricts the efferent arteriole, as well as activates systemic endocrine systems that increase pressure in the renal artery. The pressure from the heart is prioritized for juxtamedullary nephrons, that are supplied by more proximal branches from the interlobular artery, and has loops of Henle that dive deep into the medulla, and cortical nephrons receive lower pressure, and have lower glomerular filtration pressure.
# The population securely generates random numbers
The population has a protocol that allows them to generate a random numbers each period in a way that cannot be manipulated by foreign actors. It relies on a form of majority vote, but, no one can control what they vote for. They can only control that their vote is random, and know that the vote of every other person is random. This is possible by using a commit-reveal scheme, where votes are committed before the votes in the previous period have been revealed. The random number generated by majority vote each period, is used to mutate the votes in the next period. Votes contribute randomness to generators. There are as many generators as there are people, and the probability that some generator gets k hits is e^-1/k!. The generator that gets the most hits , i.e., a majority vote, wins.
The random number generator is a bit similar to proof-of-work. The population "mines" a random number, by submitting random nonces. These nonces contribute entropy to a randomly selected generator. The generator that gets the most hits , wins. The nonces are truly random, because they are mutated after they have been committed, using the random number generated in the previous cycle. It is impossible to predict what nonce will hit a winning generator.
mapping (address => bytes32) commit; // The pre-committed nonce
mapping (address => bool) reveal; // Has the person cast their number?
mapping (address => bytes32) mutation;
mapping (uint => uint) points; // Keeps tracks of score
mapping (uint => bytes32) generator; // XOR of all entropy that hit generator
uint leader; // What generator has the highest score?
It uses a game to sample who gets to submit random numbers. This game is simply, that everyone reveals their random numbers. Each random number hits another person, giving them one point. The person with the highest score, and who got the reached that score first, is selected, and the random numbers that hit them are used. The game is initialized with the random number generated in the previous game. This value is known first after people commit their encrypted random numbers. The probability that a candidate gets k points is 1/k! (multiplied by 1/e). The second highest score, will have k times more candidates than the highest score, and the probability that honest players can generate that score without the colluders is > 1 if percentageHonest>k.
# Randomization
The random number generation in Online Pseudonym Parties relies on that every person submits random entropy, and that every person votes (in a way they cannot predict or control) for the entropy submitted by a random person. This is made possible by that the list of registered people one month (who have pre-committed their entropy, but not yet revealed it) is randomized using the random number generated by the registered people the previous month.
The probability that a candidate gets k points is 1/k! (multiplied by 1/e) i.e., the probability of 2 points is /=2 less than 1 point. The probability of 3 points is /=3 less than 2 points. The probability of 4 points is /=4 less than 3 points. The highest score should on average be the value of k where k!*e is closest to population.
If it is a draw, the person who had the most points first is selected. If the person who won did not reveal a number, they are skipped and the person next in line for the win is selected.
For example, the average highest score with 8*10^9 people, will be 12.7 points (x!*e = 8*10^9, solve for x). This is not possible to get, since points are integers, so, it will be 12 points, with the occasional 13 point score. It can be calculated that on average 6 people will get 12 points, (1/(12!*e))*(8*10^9) = 6. If the colluders control either of the accounts that hold the "winning votes", they will at best be able to cast their vote as fast as they can (to be the first to get to 12 points), but, without knowing if that value is better than any of the others that will be revealed.
An example of how secure the randomization mechanism is: what if the colluding party waits until last to reveal? Then they'd get a lot of numbers to choose from? Well, the probability of a score k being reached decreases as 1/k!. With 8 billion people, 12.7 points is the norm. To reach 12 points, the average population size required is just 12!*e = 1.3 billion people. So as long as 1.3/8 = 16% honestly reveal their numbers, the colluders will at best have on average a single 13 vote to either cast, or not cast. So, they end up choosing just between two randomly selected numbers. And, this assumes a huge colluding party of upwards 50%, who'd have 50% chance of holding the "13" vote.
But what if colluders cast very early votes? Total 12 point votes in a population of 8 billion is on average 8 billion/12!*e = 8 billion/1.3 = 6.15 candidates. The colluders will at best be able to hand pick from a few random number candidates if they submit first at the winning score.
The random number generation in Online Pseudonym Parties relies on that every person submits random entropy, and that every person votes (in a way they cannot predict or control) for the entropy submitted by a random person. This is made possible by that the list of registered people one month (who have pre-committed their entropy, but not yet revealed it) is randomised using the random number generated by the registered people the previous month.
The probability that a candidate gets k points is 1/k! (multiplied by 1/e) i.e., the probability of 2 points is /=2 less than 1 point. The probability of 3 points is /=3 less than 2 points. The probability of 4 points is /=4 less than 3 points. The highest score should on average be the value of k where k!*e is closest to population.
If it is a draw, the person who had the most points first is selected. If the person who won did not reveal a number, it goes to the person with the second highest score.
For example, the highest score with 8*10^9 people, will be 12.7 points. This is not possible to get, so, it will be 12 points, with the occasional 13 point score. It can be calculated that on average 6 people will get 12 points, (1/(12!*e))*(8*10^9) = 6. If the colluders control either of the accounts that hold the "winning votes", they will at best be able to throw their vote as fast as they can (to be the first to get to 12 points), but, without knowing if that value is better than any of the others that will be revealed.
# Random number generator by a proof-of-unique-person based commit-reveal scheme
A commit-reveal scheme rewarding early reveals.
Every person has pre-committed random numbers as a hash chain. And, the people form a list, that has been randomized the previous cycle.
Then, they start to reveal a number each. Once you revealed a number, you can get ability to cast a second vote, by getting "hit" by a random number someone else reveals.
If you get "hit", you get the ability to cast one more vote (reveal one more number. ) Once you have done so, you can get "hit" again. And if you do, you get to cast one more vote (reveal one more number), and if you do, you can get hit again.
The last random number revealed by the person who got the most hits , wins, and is used as a random seed.
Those who were the first 1/sqrt(2) to reveal a number out of those with an ID 1/sqrt(2)^n of the population,
get to reveal 1+n more numbers. n is number of times it has been repeated. Maximum number of votes is 4x population.
The cycles get period/2^n time allocated. Practically, time runs out before log2(population) repetitions. Total votes possible will approximate 4x population.
The thin limb in the loop of Henle in rats has an inner diameter of 15 micron.
I have assumed for half a year that pressure must increase in the thin segment, forcing osmotic reabsorption of water.
But, the Bernouli effect says that pressure decreases as pipe diameter decreases.
Still, I think pressure must somehow increase. Because of my analysis for how tubero-glomerular feedback actually works, I assume macula densa senses osmolarity and increases GFR because the pressure is what concentrates filtrate, via osmotic reabsorption in the thin segment of the loop of Henle. So I thought:
The fourth phase of water at the surface of the thin limb, formed from glomerular filtration pressure (albeit decreased in the thin segment), the hydronium layer on it must repel from side to side of the tube. Causing same pump effect as when there is asymmetry of the fourth phase of water across a membrane. Increasing exosmotic pressure.
This also fits with that loop diuretics act by breaking down the fourth phase of water (stealing protons and destabilizing it. )
# Hypertension, endothelial tyrosine hydroxylase, and hypoxia
Endothelium expresses tyrosine hydroxylase (TH), and tyrosine hydroxylase gene expression increases with hypoxia (Sorriento, 2012). This is likely part of endocrine regulation of the heart by organs such as skeletal muscle.
High blood pressure compresses the vasa vasorum, and causes hypoxia in the vessel wall (Sacks, 1975).
Chronic high blood pressure leads to chronic hypoxia in the vessel wall, and necrosis.
Cholesterol is always present during wound healing. Correlates with macrophage presence (Bagnati, 2019).
A hypothetical disturbed feedback loop during chronic hypertension, hypoxia in vessel walls from compression upregulates TH, increases adrenaline synthesis and excretion from endothelium, increases cardiac output and contracts vascular system, increases blood pressure, increases compression-damage, upregulates TH, and so on.
# References
Sorriento, D., Santulli, G., Del Giudice, C., Anastasio, A., Trimarco, B., & Iaccarino, G. (2012). Endothelial Cells Are Able to Synthesize and Release Catecholamines Both In Vitro and In Vivo. Hypertension, 60(1), 129 136. https://doi.org/10.1161/hypertensionaha.111.189605
Sacks, A. H. (1975). The Vasa Vasorum as a Link Between Hypertension and Arteriosclerosis. Angiology, 26(5), 385 390. https://doi.org/10.1177/000331977502600503
Bagnati, M., Moreno-Moral, A., Ko, J.-H., Nicod, J., Harmston, N., Imprialou, M., Game, L., Gil, J., Petretto, E., & Behmoaras, J. (2019). Systems genetics identifies a macrophage cholesterol network associated with physiological wound healing. JCI Insight, 4(2). https://doi.org/10.1172/jci.insight.125736
# Are self-recognizing Thymus lymphocytes more central than people consider?
These days, lymphocyte receptors are believed to use instructive theory to increase affinity for foreign-antigen. It is information-theory wise a lot easier to rule out self-antigen, than to recognize specific non-self antigen. Probabilistically, 9-mer peptide fragments have > 10^11 combinations (Brusic, 1999), but self-9-mer peptides < 10^8 (Brusic, 1999), at least 10^3 easier to rule out self and probably closer to 10^4. Once self is ruled out, T-cells too could use affinity maturation. And cytotoxic, specialized T-cells develop. People say T-cell receptor does not use affinity maturation but the same was said for instructive theory in general from 1960s until pretty recently I think. If an antigen presenting cell (APC) has displayed a peptide fragment on MHC that has been inspected by a threshold of 10^n self-recognizing lymphocytes, and estimated the antigen to be foreign, it could very easily order T-cells to initiate affinity maturation-like development of T-cell receptors specific to that antigen, and have a clone of T-cells that are very good at hunting down the invader, and also very good at helping B-cell to initiate affinity maturation.
The work put in by the Thymus is said to be mostly about removing self-recognizing T-cells. But, keeping them around provides an extremely useful tool. The dogma is that keeping them around is dangerous, because they might switch to a non-self recognizing type but then have a T-cell receptor for self-antigen, and then there is some memes about how weakly self-recognizing can at the same time still be allowed, and these are then assigned to the neglected and marginalized (Corthay, 2009) suppressor or regulatory T-cells. This dogma that self-recognition is dangerous, should be central to the exploration of a more central role of self-recognizing Thymus cells. If the dogma is wrong, then my intuition is right. There is also a perfectly logical reason for a hypothetical false dogma to have developed, the risk of auto-immune disease being very real, and the threat associated with self-recognition in a world that does not tolerate independent thought.
Scalability-wise, a self-centered Thymus system is extremely efficient. The number of self T-cells necessary to verify an antigen as foreign, is proportional to the number of self-antigens that MHC can present. MHC molecules are said to form highly promiscuous peptide-binding clefts (Brusic, 1999; 2004). The number of peptides that can bind each individual HLA class I molecule was estimated at between 1000 and 10000 individual sequences (S. Stevanovic via Brusic, 2004), or up to 100000 (Sem, 2007), and and more than 2000 peptides for class II allotypes (Meydan, 2013), and each individual expresses up to six HLA class I molecules and at least that many HLA class II molecules. The so-called highly promiscuous peptide binding groove is still only capable of binding a very small fraction of all possible peptide fragments, and the fraction of self-to-foreign antigen is < 10^-3 (Brusic, 1999), so out of the 10000 or 100000 possible sequences a MHC molecule can bind, only 1 to 10 (Brusic) or 100 (Sem) are self-antigen.
The extreme efficiency of a self-centered Thymus system is that the < 10^-3 proportion of MHC antigen that are self-antigen, can be validated with 10^n redundancy by total_MHC_self_antigen * 10^n randomly sampled "self lymphocytes". T-cells are known to constantly swarm the body, millions passing through lymph nodes per hour (Hall, 1967), and if there is any validity to Brusic or Sem's estimates of MHC promiscuity, that self-antigen per MHC allele are a few dozen or a few hundred, they can be used to estimate this threshold. Mathematically, in a population of x objects, where n different types of objects exist, the probability of covering all n types probably increases non-linearly and at some multiple of n, enough objects have been sampled to satisfy a desirable probability threshold. If this threshold is 100, total self lymphocytes needed to audit antigen is between 100 and 10000, per allele (and six alleles in total), depending on Brusic or Sem's estimates.
The alternative, to find the T-cell clone specific to a foreign-antigen, that have been selected by somatic mutation, never encountered the antigen before, and not undergone clonal expansion, is 10^11 possible 9-mer peptides. That MHC is only able to present a fraction of these, cannot inform the T-cell receptors that cannot know what peptides this fraction is. 10^11 possible foreign antigen in a population of 10^12 T-cells, leaves 10 T-cells per antigen. Probabilistically, each antigen has to be scanned by 10^11 T-cells to reach same conclusion as a few thousand "self lymphocytes".
# Synapses
Brusic, V., & Zeleznikow, J. (1999). Letters in Peptide Science, 6(5/6), 313 324. https://doi.org/10.1023/a:1008948124145
Brusic, V., Bajic, V. B., & Petrovsky, N. (2004). Computational methods for prediction of T-cell epitopes a framework for modelling, testing, and applications. Methods, 34(4), 436 443. https://doi.org/10.1016/j.ymeth.2004.06.006
Corthay, A. (2009). How do Regulatory T Cells Work? Scandinavian Journal of Immunology, 70(4), 326 336. https://doi.org/10.1111/j.1365-3083.2009.02308.x
Sem, D. S. (2007). Spectral Techniques In Proteomics (1st ed.). CRC Press.
Meydan, C., Otu, H. H., & Sezerman, O. U. (2013). Prediction of peptides binding to MHC class I and II alleles by temporal motif mining. BMC bioinformatics, 14 Suppl 2(Suppl 2), S13. https://doi.org/10.1186/1471-2105-14-S2-S13
Hall, J. G. (1967). QUANTITATIVE ASPECTS OF THE RECIRCULATION OF LYMPHOCYTES; AN ANALYSIS OF DATA FROM EXPERIMENTS ON SHEEP. Quarterly Journal of Experimental Physiology and Cognate Medical Sciences, 52(1), 76 85. https://doi.org/10.1113/expphysiol.1967.sp001887
# T-cells recognize only self?
Knowing that T-cells bind to MHC and evaluate antigen peptides presented on MHC, it is possible to get cause and effect backwards. The ability to experiment with T-cell receptors is less accessible than for B-cell receptors, antibodies, since T-cell receptors rely on MHC as an intermediary that presents antigen in the form of peptide fragments. While antibodies are routinely used in immunolabeling, and clearly bind non-self antigen in the body, T-cell receptors are much less directly observed, because their targets are confined to peptide fragments presented on MHC.
# Swarm-model of T-cell function, probabilistic antigen recognition
A probabilistic antigen recognition by T-cells, means that although a T-cell could occasionally learn to recognize non-self as self, and fail to identify the foreign invader, the majority of lymph cells will be conditioned to the majority of protein in the body, which is human cells, and inspection of antigen via MHC will probabilistically tend to recognize only self, encounters with the occasional dysfunctional T-cell will be a rare probability.
B-cells recognize non-self only, and T-cells recognize self only
The "needle in a haystack" problem in the adaptive immune system is solved if T-cell receptors recognize self, and not the other way around. This also has a nice symmetry, one half of the adaptive immune system recognizes non-self, and the other half only self. Contrast.
Antigen presentation to T-cells with MHC I and II is a young science. It has not been explored that long. Younger than antibodies, since those were observable more easy. And since antibodies clearly bind to non-self, there would be a priori prejudice to assume T-cell receptors did as well.
It is known that self-antigen are fewer than non-self. This is self-evident. What is not as intuitive is that the self-antigen that MHC can present, might only be a fraction of all self-antigen peptide fragments that can be produced from the human body. And T-cells that learn to recognize self, with one self-antigen per T-cell receptor, would only have to recognize the self-antigen that MHC can present.
The upper bound for self-antigen that can be recognized by T-cell receptors, can be estimated quite easily. If MHC on average presents 10 amino acid long peptide fragments, there is 20^10 = 10^13 possible combinations. 20 being the number of amino acids. Out of these 10^13 combinations, MHC is only able to bind a fraction.
To then estimate how much of that fraction is self-antigen, the possible combinations of 10 amino acid long sequences that the human genome can encode can be delineated with the size of the human genome, 3*10^9 base pairs, maximally encoding 10^9 codons, that encode an amino acid each. If the fragments can be sliced from any point in the genome, then theoretically, any 10 amino acids from any point in the genome could be unique (since 10 amino acid long sequences can generate 10^13 combinations, a 10*10^13 = 10^14 long string of base pairs, whereas human genome is just 10^9. ) 10^9 combinations is a fraction of 0.0001 of 10^13 combinations, 10^9/10^13 = 10^-4.
The T-cell receptor diversity to recognize self becomes 10^13*fraction_MHC_can_present*10^-4 = 10^9*fraction_MHC_can_present.
During MHC presentation, the antigen would need to be verified to every single self-antigen MHC can bind, but, this might not be such a large population of T-cells.
# B-cells recognize non-self only, and T-cells recognize self only
The "needle in a haystack" problem in the adaptive immune system is solved if T-cell receptors recognize non-self, and not the other way around. This also has a nice symmetry, one half of the adaptive immune system recognizes non-self, and the other half only self. Contrast. Antigen presentation to T-cells with MHC I and II is a young science. It has not been explored that long. Younger than antibodies, since those were observable more easy. And since antibodies clearly bind to non-self, there would be a priori prejudice to assume T-cell receptors did as well. Basically, every mature T-cell, if they recognize self, would have a receptor "specific" for every self-antigen in the body, because they would have passed along them all during training and their receptor would provably not react with them. So, any T-cell could activate a B-cell. This makes it scale much easier. So, T-cell receptors can either recognize 1 (one!) single antigen out of all antigen in the universe. Or, it can recognize every (every!) single self-antigen. Scalability-wise, MCH presenting cells either have to find the 1 (one!) tiny clone of T-cells that have the unique receptor for this 1 antigen out of all possible antigen. Or, they just have to find any T-cell.
Lungs have evolved to make sure blood pressure stays up, with angiotensin II. Fits with my idea that gas exchange is osmotic, and, osmosis is H+ moving, H3O2- breaking down, e- moving, and H2O forming with external O2.
Hypoxic pulmonary vasoconstriction (HPV) reflex might also fit with osmotic gas exchange.
K+ is adsorbed to surface phase of water. This expels protons. The high concentration of free protons drive synthesis of phosphate bonds, each bond storing 2 protons. The electrical circuit formed has the anode reaction when surface water breaks down, releasing electrons, and cathode reaction when phosphate bonds break, releasing protons that combine with the electrons, to form hydrogen gas, that combines with molecular oxygen to form water, releasing a lot of heat.
Osmosis consumes and produces water
An acid-base battery will consume and produce water, while providing an electrical current (Weng, 2019). The chemical basis of this is the asymmetric distribution of hydrogen in the two compartments of an acid-base cell. The alkaline compartment has a shortage of H, it favours H2O collapsing into O2 while releasing 4 electrons, and the acidic compartment has an excess of H, and favours the production of water as long as electrons are provided from the alkaline compartment.
An acid-base battery produces its proton gradient by adding a base, such as potassium hydroxide, to one compartment, and an acid, such as hydrochloric acid, to the other. Since the proton gradient is what powers the acid-base battery, and not the mechanism used to generate it, it is reasonable to predict that other ways of generating a proton gradient should result in a similar acid-base battery, one that also consumes and produces water while releasing an electrical current.
It has recently been discovered that osmosis is driven by the generation of a proton gradient across the osmotic membrane (Zhao, 2009). Knowing that a proton gradient is what powers an acid-base battery, it can be predicted that a similar behaviour should occur from the proton gradient in osmosis. Water ought to be consumed in one compartment, and produced in the other, accompanied by an electric current.
That osmosis is powered by a proton gradient has gone undiscovered since the machinery that generates this gradient, a thin layer of an electrically polarized solid phase of water, generated from the water pushing against the sides of the container, is not visible without a microscope. This compressed ice is favoured at surfaces because it is denser than water, because it has excluded the protons that link the molecular ice sheets together in ice.
This compressed ice is inherently a proton pump because it will eject its protons away from the surface it forms against, leaving a net negative charge at the surface. This negative surface charge will force protons to transfer to the other side of the surface, if the surface is permeable to protons. It therefore provides a means to generate a proton gradient that does not rely on the addition of acid and base, and should be expected to move water in the same way an acid-base battery does.
Consider two water filled containers separated by a membrane only permeable to protons and electrons. One compartment has a pump attached to it, that can increase hydrostatic pressure in it. The other has a one-way valve, that can relieve pressure, and is filled to the rim with water so that there is minimal air inside. Applying pressure with the pump will increase the gel phase at the membrane in the pump compartment. Since the vent compartment has lower pressure, it will have a thinner adsorbed water phase layer. The gel phase excludes protons, and asymmetry in the gel layers on either side of the membrane is a motor for pumping protons across the membrane. Loss of protons from the pump compartment, causes H2O to break down into O2, releasing electrons. The electrons also transfer across the membrane, and combine with the protons to form hydrogen gas. This hydrogen gas increases the pressure in the vent compartment, and is ventilated via the one-way valve. This experiment evaporates water by applying pressure, and this can be verified or falsified by weighing the combined water mass before and after the experiment. A tiny air pocket can be left before the valve, to make it easier to see that water is not being ventilated (the O2 in this air pocket will quickly be used up in the beginning of the experiment to form a minimal amount of water, after which only H2 will be produced. )
Consider two containers separated by a membrane only permeable to protons and electrons. It makes sense that a membrane would restrict permeable to the smallest units that people usually deal with, everything else such as atoms or molecules being much bigger. The hydrostatic pressure at the membrane is higher in the compartment to the left with a taller water column. The pressure increases the adsorbed gel phase at the membrane, since this phase of water has a higher density (the reverse of pressures effect on freezing point for ice. ) This causes asymmetry of the gel phase on both sides of the membrane, propelling protons over it to even out their distribution. Electrons will follow along to balance the charge, forcing water to break down in the compartment to the left. Since there is oxygen available to the compartment to the right, water will form there. Water appears to move across the membrane.
I'm pretty sure this video shows concrete evidence for a completely new model of osmosis, https://youtu.be/zzVa_tX1OiI?t=175..
In his experiment, the ammeter is connected in series between the voltage supply and the load. The amperage (shown on the ammeter) is decreasing when he plugs the compartment that receives current, by Ohm's law, I = V/R, resistance must have increased.
What explanation is there for that the resistance increases? I suggest that O2 is acting as a cathode to complete the circuit. The electrons are combining with O2 and with the protons continuously fed from the other compartment (where the opposite reaction 4 OH- --> O2 + 2 H2O + 4 e- breaks down water to keep electrostatic neutrality, those electrons leave the load and continue to the power source. ) Plugging the tube removes O2.
The idea is that water does not move during osmosis, only protons and electrons move. https://doi.org/10.5281/zenodo.4290233.
I developed an idea over the past year, since January, that I think might have some potential. It predicts osmosis is misunderstood. https://doi.org/10.5281/zenodo.4290233
I'm pretty sure concrete evidence is seen in this video, https://www.youtube.com/watch?v=zzVa_tX1OiI. The current dies when he plugs the oxygen supply. The metal conductor does not pass through the membrane, so I assume the loss of current coming back is from loss of oxygen evolution reaction 4 OH- --> O2 + 2 H2O + 4 e-, providing the electrons, as a result of loss of H+ being consumed by production of water in first compartment (it is loss of H+ that causes surplus of OH- and the breakdown of water into dioxygen gas. )
Cauda equina as a root system to drain cerebrospinal fluid
Mammals have shortened spinal cords, ascensus medullaris (Nieuwenhuys, 1964), and their lumbar and sacral nerve roots continue within the vertebral canal as a bundle of nerves called cauda equina ( horse s tail ). Mammals are also warm blooded, and have a standard metabolic rate about an order of magnitude above the basal metabolic rate of cold blooded animals (Withers, 1992). The shortening of the spinal cord is often attributed no functional role, the lumbosacral part of the vertebral canal is claimed to be basically vestigial. That may be true, but, there could also be some other explanation. The cauda equina has some resemblance to the root system of a tree. Laurent Sakka citing a J.B. Brierley describes arachnoid villi in lumbosacral nerve roots that absorb cerebrospinal fluid and drains it into the lymphatic system. Arachnoid villi on lumbar and sacral nerve roots are also described by Weller, Kido and Welsch. The anatomical position of the cauda equina means that it would drain lymphatically directly into the cisterna chylii, and it is emptied using the respiratory pump, since it is in the abdominal coelom. Karl Bechter describes that "the total cerebrospinal fluid outflow volume at the lumbar site [along lumbar nerves] was remarkable .
The cauda equina could also drain CSF via venous system, also using respiratory pump as it drains into inferior vena cava in abdominal coelom. The vascularization of the cauda equina is often reported to be "hypovascular" (Parke, 1981, and people frequently citing Parke), but, the opposite is also reported (Kobayashi, 2000), claiming bias and false interpretations on those reporting hypovascularization.
References
Nieuwenhuys, R. (1964). [Progress in Brain Research] Organization of the Spinal Cord Volume 11 || Comparative Anatomy of the Spinal Cord. , (), 1 57. doi:10.1016/s0079-6123(08)64043-1
Withers, P. C. 1992. Comparative Animal Physiology, New York: Saunders.
L. Sakka; G. Coll; J. Chazal (2011). Anatomy and physiology of cerebrospinal fluid. , 128(6), 309 316. doi:10.1016/j.anorl.2011.03.002
Brierley JB, Field EJ, Yoffey JM. Passage of indian ink particles from the cranial subarachnoid space. J Anat 1949;83:77.
Weller, R. O., Djuanda, E., Yow, H.-Y., & Carare, R. O. (2008). Lymphatic drainage of the brain and the pathophysiology of neurological disease. Acta Neuropathologica, 117(1), 1 14. https://doi.org/10.1007/s00401-008-0457-0
Kido DK, Gomez DG, Pavese AMJ, Potts DG (1976) Human spinal arachnoid villi and granulations. Neuroradiology 11:221 228
Welch K, Pollay M (1963) The spinal arachnoid villi of the monkeys Cercopithecus aethiops sabaeus and Macaca irus. Anat Rec 145:43 48
Bechter, K., & Schmitz, B. (2014). Cerebrospinal fluid outflow along lumbar nerves and possible relevance for pain research: case report and review. Croatian medical journal, 55(4), 399 404. https://doi.org/10.3325/cmj.2014.55.399
Parke WW, Gammell K, Rothman RH. Arterial vascularization of the cauda equina.J Bone Joint Surg Am. 1981;63:53 62
Kobayashi S, Yoshizawa H, Nakai S. Experimental study on the dynamics of lumbosacral nerve root circulation.Spine (Phila Pa 1976) 2000;25:298 305
Osmosis produces water from external oxygen
The adsorbed water-phase that forms at contact zones separates water into its ionic constituents, the hydroxide forms a crystalline structure closest to the membrane, (H3O2-)n, and the protons form a layer of H3O+ on top of it. The ordering of water at contact zones is a colligative property, and is promoted in the water compartment and impaired in the salt compartment. It is the asymmetry in the adsorbed water phase on either side of a membrane that causes a transfer of protons to the hyperosmotic compartment during osmosis. The protons reorder around the combined charge of the hydroxide layer on both sides of the membrane, that acts like a motor. (Zhao, 2009; Pollack, 2013)
The loss of protons from the water compartment forces water to decompose into dioxide, there is not enough hydrogen to sustain the water. This reaction releases one electron per water, and the electrons will move towards a region of lower negative charge, the salt compartment. This electrical potential was measured by Jaques Loeb in 1921, and corroborated by Gerald Pollack in 2009.
When external oxygen is supplied to the salt compartment, it will combine with the protons and electrons that were transferred from the water compartment, and produce water. Water itself does not move across the membrane. It only appears to move.
That external oxygen is required for osmosis is a hypothesis that can be easily tested experimentally by performing a standard osmosis experiment without external oxygen in the salt compartment. The author has not done so.
References
Zhao, Q., Ovchinnikova, K., Chai, B., Yoo, H., Magula, J., & Pollack, G. H. (2009). Role of Proton Gradients in the Mechanism of Osmosis. The Journal of Physical Chemistry B, 113(31), 10708 10714. https://doi.org/10.1021/jp9021568
Pollack, G., 2013. The Fourth Phase Of Water. Seattle: Ebner and Sons.
Loeb, J. (1921). THE ORIGIN OF THE POTENTIAL DIFFERENCES RESPONSIBLE FOR ANOMALOUS OSMOSIS. Journal of General Physiology, 4(2), 213 226. https://doi.org/10.1085/jgp.4.2.213
The origin of lungs, the swim bladder as an oxygen-enriched diving system
The illustration of the swim bladder in fishes ... shows us clearly the highly important fact that an organ originally constructed for one purpose, namely, flotation, may be converted into one for a widely different purpose, namely, respiration. The swim bladder has, also, been worked in as an accessory to the auditory organs of certain fishes. All physiologists admit that the swim-bladder is homologous, or ideally similar in position and structure with the lungs of the higher vertebrate animals: hence there is no reason to doubt that the swim bladder has actually been converted into lungs, or an organ used exclusively for respiration. According to this view it may be inferred that all vertebrate animals with true lungs are descended by ordinary generation from an ancient and unknown prototype, which was furnished with a floating apparatus or swim bladder.
- Charles Darwin, On the Origin of Species by Means of Natural Selection, 1853
The origin of the lung is the story of the origin of the swim bladder. So, what is the origin of the swim bladder? Historically, it has been assumed to be an adaptation for buoyancy. While this is true, there is a second function of the swim bladder that is not as widely recognized. The swim bladder is able to adjust the blood gas ratios (Hall, 1924), an adaptation that allows for increased vertical range of movement.
The ocean is in an equilibrium with the atmosphere, and the dissolved gas is primarily nitrogen. The ocean gases are then in equilibrium with the blood and tissue of the organism. The organism consumes oxygen in cellular respiration, but not nitrogen, making nitrogen more prone to accumulate in tissue. During ascending vertical movement, the pressure exerted on the organism from the ocean decreases. This reduction in the pressure on the nitrogen that is dissolved in solution within tissues of the body, will cause bubble formation. These bubbles can damage tissues.
The evolution of the swim-bladder as an oxygen-enriched diving system, allowed organisms to reduce nitrogen in their tissues. The swim bladder does this in a way that is analogous to human divers using technology for oxygen-enriched air when diving, and it does it for the same reasons, to prevent decompression sickness.
This function of the swim bladder, an oxygen-enriched diving system, is not widely explored, and it might even be the primary selective pressure for the evolution of swim bladders, and therefore, for lungs.
References
HALL, F. G. (1924). THE FUNCTIONS OF THE SWIMBLADDER OF FISHES. The Biological Bulletin, 47(2), 79-[126]-1. https://doi.org/10.2307/1536532
This is an idea I have thought about for a few months. ATP is clearly a base, right? And, water forms a gel at contact zones, right? This gel excludes protons, and protons can be electrostatically substituted with potassium, you see this in hypo- or hyperkalemia causing intracellular and extracellular acidosis respectively. For example, in hyper- or hypo aldosteronism. What if the cell is creating an equivalent of charge separation by shifting the excluded protons from the gel and onto ATP, through substituting them with potassium? Discharge of this potential energy then releases electrical current, that ends up forming H2O from the protons released from ATP during ATP hydrolysis. This H2O then ionizes again as this "battery" recharges, by regenerating the ATP using sugar.
Aquatic organisms are bathed in water. In the same way water is pulled with particles when excreted from the kidney, water is pulled into the organism when its osmolarity increases as amino acids are degraded into HCO3- and NH4+. To the aquatic organism, there is no water cost to excrete these byproducts, water will first flow inwards to neutralize the osmotic balance, and then follow along outwards for the same reason. The terrestrial organism on the other hand will not have the inwards osmotic equilibration that aquatic organisms have. To the terrestrial organism, the byproducts from amino acid catabolism have a large cost in water. This is the reason terrestrial organisms have evolved ways to lower that cost, by turning the HCO3- and NH4+ into CO2 and urea. Urea is a weaker base than ammonia, and will free the proton on NH4+ to combine with HCO3-, forming carbon dioxide that can be exhaled with no water cost, removing 50% of the cost. Urea also combines two NH3 into a single molecule, lowering the osmotic pressure by 2x, reducing the total osmotic cost with another 25%. The end result is that only 1/4th as much water is needed.
Loop of Henle thin segment generates passive single effect in kidney
The idea is simple. The thin segment in the metanephros (the one terrestrial animals have) is homologous to thin segment in mesonephros (that aquatic animals have) and archinephros (that is a bit evolutionarily older than mesonephros). Homer Smith, the world leading authority on kidney in early 1900s, detailed this in his original work from 1935.
In mesonephros it has formed a loop that dives deep into kidney towards the papilla where urine eventually drains. This loop was discovered in 1800s by a Jacob Henle and is named after him, Henle s loop .
Since it is thin , resistance to fluid flowing into it is high. This forces the fluid to concentrate itself. That is self-evident based on standard fluid dynamics. This is what people have missed. It is a passive effect for the countercurrent multiplication. Such a mechanism has been theorized for 50 years, but, so, it is self-evident that this is what causes it. It is powered by pressure from the heart, the kidney in mammals receives 1/5th of cardiac pressure (arms, head, legs, and stomach organs get the other 4/5ths. )
This passive mechanism is then monitored by the main function-monitoring-system of the kidney, the juxtaglomerular apparatus . People think it is monitoring blood pressure basically. Like, as if animals have trouble with that.
Synapses
Smith, H. W., Thomson, K. S., Little, Brown and Company,, & McClelland and Stewart Limited,. (1953). From fish to philosopher. Boston: Little, Brown and Company.
Kokko, J. P., & Rector, F. C., Jr. (1972). Countercurrent multiplication system without active transport in inner medulla. Kidney International, 2(4), 214 223. https://doi.org/10.1038/ki.1972.97
Sands, J. M., & Layton, H. E. (2009). The Physiology of Urinary Concentration: An Update. Seminars in Nephrology, 29(3), 178 195. https://doi.org/10.1016/j.semnephrol.2009.03.008
Gilmer, G. G., Deshpande, V. G., Chou, C.-L., & Knepper, M. (2018). Flow resistance along the rat renal tubule. American Journal of Physiology-Renal Physiology, 315(5), F1398 F1405. https://doi.org/10.1152/ajprenal.00219.2018
Layton, A. T., & Layton, H. E. (2011). Countercurrent multiplication may not explain the axial osmolality gradient in the outer medulla of the rat kidney. American Journal of Physiology-Renal Physiology, 301(5), F1047 F1056. https://doi.org/10.1152/ajprenal.00620.2010
Berliner, R. W., Levinsky, N. G., Davidson, D. G., & Eden, M. (1958). Dilution and concentration of the urine and the action of antidiuretic hormone. The American Journal of Medicine, 24(5), 730 744. https://doi.org/10.1016/0002-9343(58)90377-2
The glomerular filtration reflex in the juxtaglomerular apparatus is likely monitoring the passive single effect Kokko & Rector alluded to in 1972 (Kokko, 1972; Sands, 2009). This passive osmotic multiplier is generated by the resistance peak at the thin segment that Mark Knepper has documented (Knepper, 2018), and that is self-evident based on standard fluid dynamics. Harold Layton alluded to the passive osmotic multiplier as well (Layton, 2011), and he also referenced Berliner who also alluded to the same mechanism (Berliner, 1958).
Synapses
Kokko, J. P., & Rector, F. C., Jr. (1972). Countercurrent multiplication system without active transport in inner medulla. Kidney International, 2(4), 214 223. https://doi.org/10.1038/ki.1972.97
Sands, J. M., & Layton, H. E. (2009). The Physiology of Urinary Concentration: An Update. Seminars in Nephrology, 29(3), 178 195. https://doi.org/10.1016/j.semnephrol.2009.03.008
Gilmer, G. G., Deshpande, V. G., Chou, C.-L., & Knepper, M. (2018). Flow resistance along the rat renal tubule. American Journal of Physiology-Renal Physiology, 315(5), F1398 F1405. https://doi.org/10.1152/ajprenal.00219.2018
Layton, A. T., & Layton, H. E. (2011). Countercurrent multiplication may not explain the axial osmolality gradient in the outer medulla of the rat kidney. American Journal of Physiology-Renal Physiology, 301(5), F1047 F1056. https://doi.org/10.1152/ajprenal.00620.2010
Berliner, R. W., Levinsky, N. G., Davidson, D. G., & Eden, M. (1958). Dilution and concentration of the urine and the action of antidiuretic hormone. The American Journal of Medicine, 24(5), 730 744. https://doi.org/10.1016/0002-9343(58)90377-2
The glomerular filtration reflex in the juxtaglomerular apparatus is likely monitoring the passive single effect Kokko & Rector alluded to in 1972 (Kokko, 1972; Sands, 2009). This passive osmotic multiplier is generated by the resistance peak at the thin segment that Mark Knepper has documented (Knepper, 2018), and that is self-evident based on standard fluid dynamics. Harold Layton alluded to the passive osmotic multiplier as well (Layton, 2011), and he also referenced Berliner who also alluded to the same mechanism (Berliner, 1958).
Synapses
Kokko, J. P., & Rector, F. C., Jr. (1972). Countercurrent multiplication system without active transport in inner medulla. Kidney International, 2(4), 214 223. https://doi.org/10.1038/ki.1972.97
Sands, J. M., & Layton, H. E. (2009). The Physiology of Urinary Concentration: An Update. Seminars in Nephrology, 29(3), 178 195. https://doi.org/10.1016/j.semnephrol.2009.03.008
Gilmer, G. G., Deshpande, V. G., Chou, C.-L., & Knepper, M. (2018). Flow resistance along the rat renal tubule. American Journal of Physiology-Renal Physiology, 315(5), F1398 F1405. https://doi.org/10.1152/ajprenal.00219.2018
Layton, A. T., & Layton, H. E. (2011). Countercurrent multiplication may not explain the axial osmolality gradient in the outer medulla of the rat kidney. American Journal of Physiology-Renal Physiology, 301(5), F1047 F1056. https://doi.org/10.1152/ajprenal.00620.2010
Berliner, R. W., Levinsky, N. G., Davidson, D. G., & Eden, M. (1958). Dilution and concentration of the urine and the action of antidiuretic hormone. The American Journal of Medicine, 24(5), 730 744. https://doi.org/10.1016/0002-9343(58)90377-2
<h1>The gel-phase selectively adsorbs potassium</h1>
<p>Cells have been shown to selectively adsorb potassium ions over sodium ions (Ling, 1962). The explanation for this might be that potassium (and sodium to a lesser extent) is able to replace the excluded proton. The repelling force between the lattice sheets can be overcome by a stronger attractive force, from an atom with a higher number of protons in the nucleus. Normally, the attractive force falls off rapidly down the rows of the periodic table because of increased distance to the nucleus. But in the ice crystal, the distance of attraction is not limited by the atomic radius, it is limited by the repelling force between the sheets. As long as the atomic radius is less than the repelling force between the sheets, the strength of attraction will continue to increase down the rows as well, explaining the selective adsorption of potassium ions in the cell.</p>
<h1>The gel-phase selectively adsorbs potassium</h1>
<p>Cells have been shown to selectively adsorb potassium ions over sodium ions (Ling, 1962). The explanation for this might be that potassium (and sodium to a lesser extent) is able to replace the excluded proton. The repelling force between the lattice sheets can be overcome by a stronger attractive force, from an atom with a higher number of protons in the nucleus. Normally, the attractive force falls off rapidly down the rows of the periodic table because of increased distance to the nucleus. But in the ice crystal, the distance of attraction is not limited by the atomic radius, it is limited by the repelling force between the sheets. As long as the atomic radius is less than the repelling force between the sheets, the strength of attraction will continue to increase down the rows as well, explaining the selective adsorption of potassium ions in the cell.</p>