Podcasts about h2so4

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ReferencesWe considered the complexity of the machinery to excrete ammonium in the context of research on dietary protein and how high protein intake may increase glomerular pressure and contribute to progressive renal disease (many refer to this as the “Brenner hypothesis”). Dietary protein intake and the progressive nature of kidney disease: the role of hemodynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis in aging, renal ablation, and intrinsic renal diseaseA trial that studied low protein and progression of CKD The Effects of Dietary Protein Restriction and Blood-Pressure Control on the Progression of Chronic Renal Disease(and famously provided data for the MDRD eGFR equation A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Modification of Diet in Renal Disease Study GroupWe wondered about dietary recommendations in CKD. of note, this is best done in the DKD guidelines from KDIGO Executive summary of the 2020 KDIGO Diabetes Management in CKD Guideline: evidence-based advances in monitoring and treatment.Joel mentioned this study on red meat and risk of ESKD. Red Meat Intake and Risk of ESRDWe referenced the notion of a plant-based diet. This is an excellent review by Deborah Clegg and Kathleen Hill Gallant. Plant-Based Diets in CKD : Clinical Journal of the American Society of NephrologyHere's the review that Josh mentioned on how the kidney appears to sense pH Molecular mechanisms of acid-base sensing by the kidneyRemarkably, Dr. Dale Dubin put a prize in his ECG book Free Car Prize Hidden in Textbook Read the fine print: Student wins T-birdA review of the role of the kidney in DKA: Diabetic ketoacidosis: Role of the kidney in the acid-base homeostasis re-evaluatedJosh mentioned the effects of infusing large amounts of bicarbonate The effect of prolonged administration of large doses of sodium bicarbonate in man and this study on the respiratory response to a bicarbonate infusion: The Acute Effects In Man Of A Rapid Intravenous Infusion Of Hypertonic Sodium Bicarbonate Solution. Ii. Changes In Respiration And Output Of Carbon DioxideThis is the study of acute respiratory alkalosis in dogs: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC293311/?page=1And this is the study of medical students who went to the High Alpine Research Station on the Jungfraujoch in the Swiss Alps https://www.nejm.org/doi/full/10.1056/nejm199105163242003Self explanatory! A group favorite! It Is Chloride Depletion Alkalosis, Not Contraction AlkalosisEffects of chloride and extracellular fluid volume on bicarbonate reabsorption along the nephron in metabolic alkalosis in the rat. Reassessment of the classical hypothesis of the pathogenesis of metabolic alkalosisA review of pendrin's role in volume homeostasis: The role of pendrin in blood pressure regulation | American Journal of Physiology-Renal PhysiologyInfusion of bicarbonate may lead to a decrease in respiratory stimulation but the shift of bicarbonate to the CSF may lag. Check out this review Neural Control of Breathing and CO2 Homeostasis and this classic paper Spinal-Fluid pH and Neurologic Symptoms in Systemic Acidosis.OutlineOutline: Chapter 11- Regulation of Acid-Base Balance- Introduction - Bicarb plus a proton in equilibrium with CO2 and water - Can be rearranged to HH - Importance of regulating pCO2 and HCO3 outside of this equation - Metabolism of carbs and fats results in the production of 15,000 mmol of CO2 per day - Metabolism of protein and other “substances” generates non-carbonic acids and bases - Mostly from sulfur containing methionine and cysteine - And cationic arginine and lysine - Hydrolysis of dietary phosphate that exists and H2PO4– - Source of base/alkali - Metabolism of an ionic amino acids - Glutamate and asparatate - Organic anions going through gluconeogenesis - Glutamate, Citrate and lactate - Net effect on a normal western diet 50-100 mEq of H+ per day - Homeostatic response to these acid-base loads has three stages: - Chemical buffering - Changes in ventilation - Changes in H+ excretion - Example of H2SO4 from oxidation of sulfur containing AA - Drop in bicarb will stimulate renal acid secretion - Nice table of normal cid-base values, arterial and venous- Great 6 bullet points of acid-base on page 328 - Kidneys must excrete 50-100 of non-carbonic acid daily - This occurs by H secretion, but mechanisms change by area of nephron - Not excreted as free H+ due to minimal urine pH being equivalent to 0.05 mmol/L - No H+ can be excreted until virtually all of th filtered bicarb is reabsorbed - Secreted H+ must bind buffers (phosphate, NH3, cr) - PH is main stimulus for H secretion, though K, aldo and volume can affect this.- Renal Hydrogen excretion - Critical to understand that loss of bicarb is like addition of hydrogen to the body - So all bicarb must be reabsorbed before dietary H load can be secreted - GFR of 125 and bicarb of 24 results in 4300 mEq of bicarb to be reabsorbed daily - Reabsorption of bicarb and secretion of H involve H secretion from tubular cells into the lumen. - Thee initial points need to be emphasized - Secreted H+ ion are generated from dissociation of H2O - Also creates OH ion - Which combine with CO2 to form HCO3 with the help of zinc containing intracellular carbonic anhydrase. - This is how the secretion of H+ which creates an OH ultimately produces HCO3 - Different mechanisms for proximal and distal acidification - NET ACID EXCRETION - Free H+ is negligible - So net H+ is TA + NH4 – HCO3 loss - Unusually equal to net H+ load, 50-100 mEq/day - Can bump up to 300 mEq/day if acid production is increased - Net acid excretion can go negative following a bicarb or citrate load - Proximal Acidification - Na-H antiporter (or exchanger) in luminal membrane - Basolateral membrane has a 3 HCO3 Na cotransporter - This is electrogenic with 3 anions going out and only one cation - The Na-H antiporter also works in the thick ascending limb of LOH - How about this, there is also a H-ATPase just like found in the intercalated cells in the proximal tubule and is responsible for about a third of H secretion - And similarly there is also. HCO3 Cl exchanger (pendrin-like) in the proximal tubule - Footnote says the Na- 3HCO3 cotransporter (which moves sodium against chemical gradient NS uses negative charge inside cell to power it) is important for sensing acid-base changes in the cell. - Distal acidification - Occurs in intercalated cells of of cortical and medullary collecting tubule - Three main characteristics - H secretion via active secretory pumps in the luminal membrane - Both H-ATPase and H-K ATPase - H- K ATPase is an exchange pump, k reabsorption - H-K exchange may be more important in hypokalemia rather than in acid-base balance - Whole paragraph on how a Na-H exchanger couldn't work because the gradient that H has to be pumped up is too big. - H-ATPase work like vasopressin with premise H-ATPase sitting on endocarditis vesicles a=which are then inserted into the membrane. Alkalosis causes them to be recycled out of the membrane. - H secretory cells do not transport Na since they have few luminal Na channels, but are assisted by the lumen negative tubule from eNaC. - Minimizes back diffusion of H+ and promotes bicarb resorption - Bicarbonate leaves the cell through HCO3-Cl exchanger which uses the low intracellular Cl concentration to power this process. - Same molecule is found on RBC where it is called band 3 protein - Figure 11-5 is interesting - Bicarbonate resorption - 90% in the first 1-22 mm of the proximal tubule (how long is the proximal tubule?) - Lots of Na-H exchangers and I handed permeability to HCO3 (permeability where?) - Last 10% happens distally mostly TAL LOH via Na-H exchange - And the last little bit int he outer medullary collecting duct. - Carbonic anhydrase and disequilibrium pH - CA plays central role in HCO3 reabsorption - After H is secreted in the proximal tubule it combines with HCO# to form carbonic acid. CA then dehydrates it to CO2 and H2O. (Step 2) - Constantly moving carbonic acid to CO2 and H2O keeps hydrogen combining with HCO3 since the product is rapidly consumed. - This can be demonstrated by the minimal fall in luminal pH - That is important so there is not a luminal gradient for H to overcome in the Na-H exchanger (this is why we need a H-ATPase later) - CA inhibitors that are limited tot he extracellular compartment can impair HCO3 reabsorption by 80%. - CA is found in S1, S2 but not S3 segment. See consequence in figure 11-6. - The disequilibrium comes from areas where there is no CA, the HH formula falls down because one of the assumptions of that formula is that H2CO3 (carbonic acid) is a transient actor, but without CA it is not and can accumulate, so the pKa is not 6.1. - Bicarbonate secretion - Type B intercalated cells - H-ATPase polarity reversed - HCO3 Cl exchanger faces the apical rather than basolateral membrane- Titratable acidity - Weak acids are filtered at the glom and act as buffers in the urine. - HPO4 has PKA of 6.8 making it ideal - Creatinine (pKa 4.97) and uric acid (pKa 5.75) also contribute - Under normal cinditions TA buffers 10-40 mEa of H per day - Does an example of HPO4(2-):H2PO4 (1-) which exists 4:1 at pH of 7.4 (glomerular filtrate) - So for 50 mEq of Phos 40 is HPO4 and 10 is H2PO4 - When pH drops to 6.8 then the ratio is 1:1 so for 50 - So the 50 mEq is 25 and 25, so this buffered an additional 15 mEq of H while the free H+ concentration increased from 40 to 160 nanomol/L so over 99.99% of secreted H was buffered - When pH drops to 4.8 ratio is 1:100 so almost all 50 mEq of phos is H2PO4 and 39.5 mEq of H are buffered. - Acid loading decreases phosphate reabsorption so more is there to act as TA. - Decreases activity of Na-phosphate cotransporter - DKA provides a novel weak acid/buffer beta-hydroxybutyrate (pKa 4.8) which buffers significant amount of acid (50 mEq/d).- Ammonium Excretion - Ability to excrete H+ as ammonium ions adds an important amount of flexibility to renal acid-base regulation - NH3 and NH4 production and excretion can be varied according to physiologic need. - Starts with NH3 production in tubular cells - NH3, since it is neutral then diffuses into the tubule where it is acidified by the low pH to NH4+ - NH4+ is ionized and cannot cross back into the tubule cells(it is trapped in the tubular fluid) - This is important for it acting as an important buffer eve though the pKa is 9.0 - At pH of 6.0 the ratio of NH3 to NH4 is 1:1000 - As the neutral NH3 is converted to NH4 more NH3 from theintracellular compartment flows into the tubular fluid replacing the lost NH3. Rinse wash repeat. - This is an over simplification and that there are threemajor steps - NH4 is produced in early proximal tubular cells - Luminal NH4 is partially reabsorbed in the TAL and theNH3 is then recycled within the renal medulla - The medullary interstitial NH3 reaches highconcentrations that allow NH3 to diffuse into the tubular lumen in the medullary collecting tubule where it is trapped as NH4 by secreted H+ - NH4 production from Glutamine which converts to NH4 and glutamate - Glutamate is converted to alpha-ketoglutarate - Alpha ketoglutarate is converted to 2 HCO3 ions - HCO3 sent to systemic circulation by Na-3 HCO3 transporter - NH4 then secreted via Na-H exchanger into the lumen - NH4 is then reabsorbed by NaK2Cl transporter in TAL - NH4 substitutes for K - Once reabsorbed the higher intracellular pH causes NH4 to convert to NH3 and the H that is removed is secreted through Na-H exchanger to scavenge the last of the filtered bicarb. - NH3 diffuses out of the tubular cells into the interstitium - NH4 reabsorption in the TAL is suppressed by hyperkalemia and stimulated by chronic metabolic acidosis - NH4 recycling promotes acid clearance - The collecting tubule has a very low NH3 concentration - This promotes diffusion of NH3 into the collecting duct - NH3 that goes there is rapidly converted to NH4 allowing more NH3 to diffuse in. - Response to changes in pH - Increased ammonium excretion with two processes - Increased proximal NH4 production - This is delayed 24 hours to 2-3 days depending on which enzyme you look at - Decreased urine pH increases diffusion of ammonia into the MCD - Occurs with in hours of an acid load - Peak ammonium excretion takes 5-6 days! (Fig 11-10) - Glutamine is picked up from tubular fluid but with acidosis get Na dependent peritublar capillary glutamine scavenging too - Glutamine metabolism is pH dependent with increase with academia and decrease with alkalemia - NH4 excretion can go from 30-40 mEq/day to > 300 with severe metabolic acidosis (38 NaBicarb tabs) - Says each NH4 produces equimolar generation of HCO3 but I thought it was two bicarb for every alpha ketoglutarate?- The importance of urine pH - Though the total amount of hydrogren cleared by urine pH is insignificant, an acidic urine pH is essential for driving the reactions of TA and NH4 forward.- Regulation of renal hydrogen excretion - Net acid excretion vary inverse with extracellular pH - Academia triggers proximal and distal acidification - Proximally this: - Increased Na-H exchange - Increased luminal H-ATPase activity - Increased Na:3HCO3 cotransporter on the basolateral membrane - Increased NH4 production from glutamine - In the collecting tubules - Increased H-ATPase - Reduction of tubular pH promotes diffusion of NH3 which gets converted to NH4…ION TRAPPING - Extracellular pH affects net acid excretion through its affect on intracellular pH - This happens directly with respiratory disorders due to movement of CO2 through the lipid bilayer - In metabolic disorders a low extracellular bicarb with cause bicarb to diffuse out of the cell passively, this lowers intracellular pH - If you manipulate both low pCO2 and low Bicarb to keep pH stable there will be no change in the intracellular pH and there is no change in renal handling of acid. It is intracellular pH dependent - Metabolic acidosis - Ramps up net acid secretion - Starts within 24 hours and peaks after 5-6 days - Increase net secretion comes from NH4 - Phosphate is generally limited by diet - in DKA titratable acid can be ramped up - Metabolic alkalosis - Alkaline extracellular pH - Increased bicarb excretion - Decrease reabsorption - HCO3 secretion (pendrin) in cortical collecting tubule - Occurs in cortical intercalated cells able to insert H-ATPase in basolateral cells (rather than luminal membrane) - Normal subjects are able to secrete 1000 mmol/day of bicarb - Maintenance of metabolic alkalosis requires a defect which forces the renal resorption of bicarb - This can be chloride/volume deficiency - Hypokalemia - Hyperaldosteronism - Respiratory acidosis and alkalosis - PCO2 via its effect on intracellular pH is an important determinant of renal acid handling - Ratios he uses: - 3.5 per 10 for respiratory acidosis - 5 per 10 for respiratory alkalosis - Interesting paragraph contrasting the response to chronic metabolic acidosis vs chronic respiratory acidosis - Less urinary ammonium in respiratory acidosis - Major differences in proximal tubule cell pH - In metabolic acidosis there is decreased bicarb load so less to be reabsorbed proximally - In respiratory acidosis the increased serum bicarb increases the amount of bicarb that must be reabsorbed proximally - The increased activity of Na-H antiporter returns tubular cell pH to normal and prevents it from creating increased urinary ammonium - Mentions that weirdly more mRNA for H-Na antiporter in metabolic acidosis than in respiratory acidosis - Net hydrogen excretion varies with effective circulating volume - Starts with bicarb infusions - Normally Tm at 26 - But if you volume deplete the patient with diuretics first this increases to 35+ - Four factors explain this increased Tm for bicarb with volume deficiency - Reduced GFR - Activation of RAAS - Ang2 stim H-Na antiporter proximally - Ang2 also stimulates Na-3HCO3 cotransporter on basolateral membrane - Aldosterone stimulates H-ATPase in distal nephron - ALdo stimulates Cl HCO3 exchanger on basolateral membrane - Aldo stimulates eNaC producing tubular lumen negative charge to allow H secretion to occur and prevents back diffusion - Hypochloremia - Increases H secretion by both Na-dependent and Na-independent methods - If Na is 140 and Cl is 115, only 115 of Na can be reabsorbed as NaCl, the remainder must be reabsorbed with HCO3 or associated with secretion of K or H to maintained electro neutrality - This is enhanced with hypochloridemia - Concurrent hypokalemia - Changes in K lead to trans cellular shifts that affect inctracellular pH - Hypokalemia causes K out, H in and in the tubular cell the cell acts if there is systemic acidosis and increases H secretion (and bicarbonate resorption) - PTH - Decreases proximal HCO3 resorption - Primary HyperCard as cause of type 2 RTA - Does acidosis stim PTH or does PTH stim net acid excretion

Z osvoboditvijo izpod jarma nacifašizma se je ovrednotil tudi eden od najbolj neposrednih izrazov ljudskega odpora – partizanska zborovska pesem. Številni pevski sestavi so v svoj repertoar uvrščali vsaj nekaj borbenih pesmi, obstoječi partizanski zbori pa so svojo ponudbo posodabljali segajoč po bogati zakladnici svetovne družbenopolitično angažirane pesmi. Vloga in pomen uporniške pesmi v današnjih časih je izhodišče pogovora, ki je nastal v rednem mesečnem sodelovanju Programa Ars, Radia Trst A in slovenskega programa ORF Celovec. Neposredni vzgib za pogovor pa izhaja iz nedavne 50-letnice neprekinjenega delovanja Tržaškega partizanskega pevskega zbora Pinko Tomažič. V studiu v Trstu ga zastopa dirigentka Pia Cah. Z uporniškimi stihi se med drugim ukvarja tudi sogovornik v ljubljanskem studiu dr. Igor Saksida, urednik antologije H2SO4 – zbirka slovenske uporniške poezije. V celovškem studiu se nam pridružuje dolgoletni pevec v številnih zborih na avstrijskem in slovenskem Koroškem ter pozoren spremljevalec nekajletne izkušnje koroškega partizanskega zbora Franc Kuežnik. Pogovor vodi Pavel Volk. FOTO: Wikipedija

Sadece zenginlerin yerinden izleyebildiği turnuva olan Monte Carlo Masters başladı. Maçlar Tivibu Spor'da. Ana tabloyu yorumladık, Monte Carlo tarihine daldık. Ve haftanın şampiyonlarını konuştuk. Marakeş'teki turnuvanın ismi bizi ortaokul kimya dersine götürdü.

ReferencesWe considered the effect of a high protein diet and potential metabolic acidosis on kidney function. This review is of interest by Donald Wesson, a champion for addressing this issue and limiting animal protein: Mechanisms of Metabolic Acidosis-Induced Kidney Injury in Chronic Kidney DiseaseHostetter explored the effect of a high protein diet in the remnant kidney model with 1 ¾ nephrectomy. Rats with reduced dietary acid load (by bicarbonate supplementation) had less tubular damage. Chronic effects of dietary protein in the rat with intact and reduced renal massWesson explored treatment of metabolic acidosis in humans with stage 3 CKD in this study. Treatment of metabolic acidosis in patients with stage 3 chronic kidney disease with fruits and vegetables or oral bicarbonate reduces urine angiotensinogen and preserves glomerular filtration rateIn addition to the effect of metabolic acidosis from a diet high in animal protein, this diet also leads to hyperfiltration. This was demonstrated in normal subjects; ingesting a protein diet had a significantly higher creatinine clearance than a comparable group of normal subjects ingesting a vegetarian diet. Renal functional reserve in humans: Effect of protein intake on glomerular filtration rate.This finding has been implicated in Brenner's theory regarding hyperfiltration: The hyperfiltration theory: a paradigm shift in nephrologyOne of multiple publications from Dr. Nimrat Goraya whom Joel mentioned in the voice over: Dietary Protein as Kidney Protection: Quality or Quantity?We wondered about the time course in buffering a high protein meal (and its subsequent acid load on ventilation) and Amy found this report:Effect of Protein Intake on Ventilatory Drive | Anesthesiology | American Society of Anesthesiologists Roger mentioned that the need for acetate to balance the acid from amino acids in parenteral nutrition was identified in pediatrics perhaps because infants may have reduced ability to generate acid. Randomised controlled trial of acetate in preterm neonates receiving parenteral nutrition - PMCHe also recommended an excellent review on the complications of parenteral nutrition by Knochel https://www.kidney-international.org/action/showPdf?pii=S0085-2538%2815%2933384-6 which explained that when the infused amino acids disproportionately include cationic amino acids, metabolism led to H+ production. This is typically mitigated by preparing a solution that is balanced by acetate. Amy mentioned this study that explored the effect of protein intake on ventilation: Effect of Protein Intake on Ventilatory Drive | Anesthesiology | American Society of AnesthesiologistsAnna and Amy reminisced about a Skeleton Key Group Case from the renal fellow network Skeleton Key Group: Electrolyte Case #7JC wondered about isolated defects in the proximal tubule and an example is found here: Mutations in SLC4A4 cause permanent isolated proximal renal tubular acidosis with ocular abnormalitiesAnna's Voiceover re: Gastric neobladder → metabolic alkalosis and yes, dysuria. The physiology of gastrocystoplasty: once a stomach, always a stomach but not as common as you might think Gastrocystoplasty: long-term complications in 22 patientsSjögren's syndrome has been associated with acquired distal RTA and in some cases, an absence of the H+ ATPase, presumably from autoantibodies to this transporter. Here's a case report: Absence of H(+)-ATPase in cortical collecting tubules of a patient with Sjogren's syndrome and distal renal tubular acidosisCan't get enough disequilibrium pH? Check this out- Spontaneous luminal disequilibrium pH in S3 proximal tubules. Role in ammonia and bicarbonate transport.Acetazolamide secretion was studied in this report Concentration-dependent tubular secretion of acetazolamide and its inhibition by salicylic acid in the isolated perfused rat kidney. | Drug Metabolism & DispositionIn this excellent review, David Goldfarb tackles the challenging case of a A Woman with Recurrent Calcium Phosphate Kidney Stones (spoiler alert, many of these patients have incomplete distal RTA and this problem is hard to treat). Molecular mechanisms of renal ammonia transport excellent review from David Winer and Lee Hamm. OutlineOutline: Chapter 11- Regulation of Acid-Base Balance- Introduction - Bicarb plus a proton in equilibrium with CO2 and water - Can be rearranged to HH - Importance of regulating pCO2 and HCO3 outside of this equation - Metabolism of carbs and fats results in the production of 15,000 mmol of CO2 per day - Metabolism of protein and other “substances” generates non-carbonic acids and bases - Mostly from sulfur containing methionine and cysteine - And cationic arginine and lysine - Hydrolysis of dietary phosphate that exists and H2PO4– - Source of base/alkali - Metabolism of an ionic amino acids - Glutamate and asparatate - Organic anions going through gluconeogenesis - Glutamate, Citrate and lactate - Net effect on a normal western diet 50-100 mEq of H+ per day - Homeostatic response to these acid-base loads has three stages: - Chemical buffering - Changes in ventilation - Changes in H+ excretion - Example of H2SO4 from oxidation of sulfur containing AA - Drop in bicarb will stimulate renal acid secretion - Nice table of normal cid-base values, arterial and venous- Great 6 bullet points of acid-base on page 328 - Kidneys must excrete 50-100 of non-carbonic acid daily - This occurs by H secretion, but mechanisms change by area of nephron - Not excreted as free H+ due to minimal urine pH being equivalent to 0.05 mmol/L - No H+ can be excreted until virtually all of th filtered bicarb is reabsorbed - Secreted H+ must bind buffers (phosphate, NH3, cr) - PH is main stimulus for H secretion, though K, aldo and volume can affect this.- Renal Hydrogen excretion - Critical to understand that loss of bicarb is like addition of hydrogen to the body - So all bicarb must be reabsorbed before dietary H load can be secreted - GFR of 125 and bicarb of 24 results in 4300 mEq of bicarb to be reabsorbed daily - Reabsorption of bicarb and secretion of H involve H secretion from tubular cells into the lumen. - Thee initial points need to be emphasized - Secreted H+ ion are generated from dissociation of H2O - Also creates OH ion - Which combine with CO2 to form HCO3 with the help of zinc containing intracellular carbonic anhydrase. - This is how the secretion of H+ which creates an OH ultimately produces HCO3 - Different mechanisms for proximal and distal acidification - NET ACID EXCRETION - Free H+ is negligible - So net H+ is TA + NH4 – HCO3 loss - Unusually equal to net H+ load, 50-100 mEq/day - Can bump up to 300 mEq/day if acid production is increased - Net acid excretion can go negative following a bicarb or citrate load - Proximal Acidification - Na-H antiporter (or exchanger) in luminal membrane - Basolateral membrane has a 3 HCO3 Na cotransporter - This is electrogenic with 3 anions going out and only one cation - The Na-H antiporter also works in the thick ascending limb of LOH - How about this, there is also a H-ATPase just like found in the intercalated cells in the proximal tubule and is responsible for about a third of H secretion - And similarly there is also. HCO3 Cl exchanger (pendrin-like) in the proximal tubule - Footnote says the Na- 3HCO3 cotransporter (which moves sodium against chemical gradient NS uses negative charge inside cell to power it) is important for sensing acid-base changes in the cell. - Distal acidification - Occurs in intercalated cells of of cortical and medullary collecting tubule - Three main characteristics - H secretion via active secretory pumps in the luminal membrane - Both H-ATPase and H-K ATPase - H- K ATPase is an exchange pump, k reabsorption - H-K exchange may be more important in hypokalemia rather than in acid-base balance - Whole paragraph on how a Na-H exchanger couldn't work because the gradient that H has to be pumped up is too big. - H-ATPase work like vasopressin with premise H-ATPase sitting on endocarditis vesicles a=which are then inserted into the membrane. Alkalosis causes them to be recycled out of the membrane. - H secretory cells do not transport Na since they have few luminal Na channels, but are assisted by the lumen negative tubule from eNaC. - Minimizes back diffusion of H+ and promotes bicarb resorption - Bicarbonate leaves the cell through HCO3-Cl exchanger which uses the low intracellular Cl concentration to power this process. - Same molecule is found on RBC where it is called band 3 protein - Figure 11-5 is interesting - Bicarbonate resorption - 90% in the first 1-22 mm of the proximal tubule (how long is the proximal tubule?) - Lots of Na-H exchangers and I handed permeability to HCO3 (permeability where?) - Last 10% happens distally mostly TAL LOH via Na-H exchange - And the last little bit int he outer medullary collecting duct. - Carbonic anhydrase and disequilibrium pH - CA plays central role in HCO3 reabsorption - After H is secreted in the proximal tubule it combines with HCO# to form carbonic acid. CA then dehydrates it to CO2 and H2O. (Step 2) - Constantly moving carbonic acid to CO2 and H2O keeps hydrogen combining with HCO3 since the product is rapidly consumed. - This can be demonstrated by the minimal fall in luminal pH - That is important so there is not a luminal gradient for H to overcome in the Na-H exchanger (this is why we need a H-ATPase later) - CA inhibitors that are limited tot he extracellular compartment can impair HCO3 reabsorption by 80%. - CA is found in S1, S2 but not S3 segment. See consequence in figure 11-6. - The disequilibrium comes from areas where there is no CA, the HH formula falls down because one of the assumptions of that formula is that H2CO3 (carbonic acid) is a transient actor, but without CA it is not and can accumulate, so the pKa is not 6.1. - Bicarbonate secretion - Type B intercalated cells - H-ATPase polarity reversed - HCO3 Cl exchanger faces the apical rather than basolateral membrane- Titratable acidity - Weak acids are filtered at the glom and act as buffers in the urine. - HPO4 has PKA of 6.8 making it ideal - Creatinine (pKa 4.97) and uric acid (pKa 5.75) also contribute - Under normal cinditions TA buffers 10-40 mEa of H per day - Does an example of HPO4(2-):H2PO4 (1-) which exists 4:1 at pH of 7.4 (glomerular filtrate) - So for 50 mEq of Phos 40 is HPO4 and 10 is H2PO4 - When pH drops to 6.8 then the ratio is 1:1 so for 50 - So the 50 mEq is 25 and 25, so this buffered an additional 15 mEq of H while the free H+ concentration increased from 40 to 160 nanomol/L so over 99.99% of secreted H was buffered - When pH drops to 4.8 ratio is 1:100 so almost all 50 mEq of phos is H2PO4 and 39.5 mEq of H are buffered. - Acid loading decreases phosphate reabsorption so more is there to act as TA. - Decreases activity of Na-phosphate cotransporter - DKA provides a novel weak acid/buffer beta-hydroxybutyrate (pKa 4.8) which buffers significant amount of acid (50 mEq/d).- Ammonium Excretion - Ability to excrete H+ as ammonium ions adds an important amount of flexibility to renal acid-base regulation - NH3 and NH4 production and excretion can be varied according to physiologic need. - Starts with NH3 production in tubular cells - NH3, since it is neutral then diffuses into the tubule where it is acidified by the low pH to NH4+ - NH4+ is ionized and cannot cross back into the tubule cells(it is trapped in the tubular fluid) - This is important for it acting as an important buffer eve though the pKa is 9.0 - At pH of 6.0 the ratio of NH3 to NH4 is 1:1000 - As the neutral NH3 is converted to NH4 more NH3 from theintracellular compartment flows into the tubular fluid replacing the lost NH3. Rinse wash repeat. - This is an over simplification and that there are threemajor steps - NH4 is produced in early proximal tubular cells - Luminal NH4 is partially reabsorbed in the TAL and theNH3 is then recycled within the renal medulla - The medullary interstitial NH3 reaches highconcentrations that allow NH3 to diffuse into the tubular lumen in the medullary collecting tubule where it is trapped as NH4 by secreted H+ - NH4 production from Glutamine which converts to NH4 and glutamate - Glutamate is converted to alpha-ketoglutarate - Alpha ketoglutarate is converted to 2 HCO3 ions - HCO3 sent to systemic circulation by Na-3 HCO3 transporter - NH4 then secreted via Na-H exchanger into the lumen - NH4 is then reabsorbed by NaK2Cl transporter in TAL - NH4 substitutes for K - Once reabsorbed the higher intracellular pH causes NH4 to convert to NH3 and the H that is removed is secreted through Na-H exchanger to scavenge the last of the filtered bicarb. - NH3 diffuses out of the tubular cells into the interstitium - NH4 reabsorption in the TAL is suppressed by hyperkalemia and stimulated by chronic metabolic acidosis - NH4 recycling promotes acid clearance - The collecting tubule has a very low NH3 concentration - This promotes diffusion of NH3 into the collecting duct - NH3 that goes there is rapidly converted to NH4 allowing more NH3 to diffuse in. - Response to changes in pH - Increased ammonium excretion with two processes - Increased proximal NH4 production - This is delayed 24 hours to 2-3 days depending on which enzyme you look at - Decreased urine pH increases diffusion of ammonia into the MCD - Occurs with in hours of an acid load - Peak ammonium excretion takes 5-6 days! (Fig 11-10) - Glutamine is picked up from tubular fluid but with acidosis get Na dependent peritublar capillary glutamine scavenging too - Glutamine metabolism is pH dependent with increase with academia and decrease with alkalemia - NH4 excretion can go from 30-40 mEq/day to > 300 with severe metabolic acidosis (38 NaBicarb tabs) - Says each NH4 produces equimolar generation of HCO3 but I thought it was two bicarb for every alpha ketoglutarate?- The importance of urine pH - Though the total amount of hydrogren cleared by urine pH is insignificant, an acidic urine pH is essential for driving the reactions of TA and NH4 forward.- Regulation of renal hydrogen excretion - Net acid excretion vary inverse with extracellular pH - Academia triggers proximal and distal acidification - Proximally this: - Increased Na-H exchange - Increased luminal H-ATPase activity - Increased Na:3HCO3 cotransporter on the basolateral membrane - Increased NH4 production from glutamine - In the collecting tubules - Increased H-ATPase - Reduction of tubular pH promotes diffusion of NH3 which gets converted to NH4…ION TRAPPING - Extracellular pH affects net acid excretion through its affect on intracellular pH - This happens directly with respiratory disorders due to movement of CO2 through the lipid bilayer - In metabolic disorders a low extracellular bicarb with cause bicarb to diffuse out of the cell passively, this lowers intracellular pH - If you manipulate both low pCO2 and low Bicarb to keep pH stable there will be no change in the intracellular pH and there is no change in renal handling of acid. It is intracellular pH dependent - Metabolic acidosis - Ramps up net acid secretion - Starts within 24 hours and peaks after 5-6 days - Increase net secretion comes from NH4 - Phosphate is generally limited by diet - in DKA titratable acid can be ramped up - Metabolic alkalosis - Alkaline extracellular pH - Increased bicarb excretion - Decrease reabsorption - HCO3 secretion (pendrin) in cortical collecting tubule - Occurs in cortical intercalated cells able to insert H-ATPase in basolateral cells (rather than luminal membrane) - Normal subjects are able to secrete 1000 mmol/day of bicarb - Maintenance of metabolic alkalosis requires a defect which forces the renal resorption of bicarb - This can be chloride/volume deficiency - Hypokalemia - Hyperaldosteronism - Respiratory acidosis and alkalosis - PCO2 via its effect on intracellular pH is an important determinant of renal acid handling - Ratios he uses: - 3.5 per 10 for respiratory acidosis - 5 per 10 for respiratory alkalosis - Interesting paragraph contrasting the response to chronic metabolic acidosis vs chronic respiratory acidosis - Less urinary ammonium in respiratory acidosis - Major differences in proximal tubule cell pH - In metabolic acidosis there is decreased bicarb load so less to be reabsorbed proximally - In respiratory acidosis the increased serum bicarb increases the amount of bicarb that must be reabsorbed proximally - The increased activity of Na-H antiporter returns tubular cell pH to normal and prevents it from creating increased urinary ammonium - Mentions that weirdly more mRNA for H-Na antiporter in metabolic acidosis than in respiratory acidosis - Net hydrogen excretion varies with effective circulating volume - Starts with bicarb infusions - Normally Tm at 26 - But if you volume deplete the patient with diuretics first this increases to 35+ - Four factors explain this increased Tm for bicarb with volume deficiency - Reduced GFR - Activation of RAAS - Ang2 stim H-Na antiporter proximally - Ang2 also stimulates Na-3HCO3 cotransporter on basolateral membrane - Aldosterone stimulates H-ATPase in distal nephron - ALdo stimulates Cl HCO3 exchanger on basolateral membrane - Aldo stimulates eNaC producing tubular lumen negative charge to allow H secretion to occur and prevents back diffusion - Hypochloremia - Increases H secretion by both Na-dependent and Na-independent methods - If Na is 140 and Cl is 115, only 115 of Na can be reabsorbed as NaCl, the remainder must be reabsorbed with HCO3 or associated with secretion of K or H to maintained electro neutrality - This is enhanced with hypochloridemia - Concurrent hypokalemia - Changes in K lead to trans cellular shifts that affect inctracellular pH - Hypokalemia causes K out, H in and in the tubular cell the cell acts if there is systemic acidosis and increases H secretion (and bicarbonate resorption) - PTH - Decreases proximal HCO3 resorption - Primary HyperCard as cause of type 2 RTA - Does acidosis stim PTH or does PTH stim net acid excretion

a train-hopping modern-day troubadour, rooted in folk and americana. Birmingham born, street kid superstar that's gutter punk certified. ************************************************************************************************************************************** Shop and earn with Fierce Manson at https://www.everra.com/store/fiercem

References for Chapter 10We did not mention many references in our discussion today but our listeners may enjoy some of the references below. Effects of pH on Potassium: New Explanations for Old Observations - PMC although the focus of this article is on potassium, this elegant review by Aronson and Giebisch reviews intracellular shifts as it relates to pH and K+.Josh swooned for Figure 10-1 is this right? Which figure was it? which shows the relationship between [H+] and pH. You can find this figure in the original reference from Halperin ML and others, Figure 1 here. Factors That Control the Effect of pH on Glycolysis in Leukocytes Here's Leticia Rolon's favorite Henderson-Hasselbalch calculator website: ​​Henderson-Hasselbalch Calculator | Buffer Solutions [hint! for this site, use the bicarbonate (or “total CO2”) for A- and PCO2 for the HA] There's also a cooking tab for converting units! Fundamentals of Arterial Blood Gas Interpretation - PMC this review published posthumously from the late but beloved Jerry Yee and his group at Henry Ford Hospital, explores the details and underpinnings of our understandings of arterial blood gas interpretation (and this also addresses how our colleagues in clinical chemistry measure total CO2 - which JC referenced- but JC said “machine” and our colleagues prefer the word “instrument.”)Amy went deep on bicarbonate in respiratory acidosis. Here are her refs:Sodium bicarbonate therapy for acute respiratory acidosisSodium Bicarbonate in Respiratory AcidosisBicarbonate therapy in severe metabolic acidosisEffect of Intravenous Sodium Bicarbonate on Ventilation, Gas Exchange, and Acid-Base Balance in Patients with Chronic Pulmonary InsufficiencyBicarbonate Therapy in Severe Metabolic Acidosis | American Society of Nephrology this review article from Sabatini and Kurtzman addresses the issues regarding bicarbonate therapy including theoretical intracellular acidosis. Bicarbonate in DKA? Don't do it: Bicarbonate in diabetic ketoacidosis - a systematic review Here's a review from Bushinsky and Krieger on the effect acidosis on bone https://www.sciencedirect.com/science/article/abs/pii/S0085253822002174Here is the primary resource that Anna used in here investigation of meat replacements Nutritional Composition of Novel Plant-Based Meat Alternatives and Traditional Animal-Based MeatsWe enjoyed this paper that Dr. Rose references from the Journal of Clinical Investigation 1955 in which investigators infused HCl into nephrectomized dogs and observed changes in extracellular ions. https://www.jci.org/articles/view/103073/pdWe wondered about the amino acids/protein in some available meat alternatives they are explored in this article in the journal Amino Acids: Protein content and amino acid composition of commercially available plant-based protein isolates - PMC and you may enjoy this exploration of the nutritional value of these foods: Full article: Examination of the nutritional composition of alternative beef burgers available in the United StatesOutlineChapter 10: Acid-Base Physiology - H concentration regulated tightly - Normal H+ is 40 nm/L - This one millionth the concentration of Na and K - It needs to be this dilute because H+ fucks shit up - Especially proteins - Cool foot note H+ actually exists as H3O+ - Under normal conditions the H+ concentration varies little from normal due to three steps - Chemical buffering by extracellular and intracellular bufffers - Control of partial pressure of CO2 by alterations of alveolar ventilation - Control of plasma bicarbonate by changes in renal H+ excretion - Acid and bases - Use definition by Bronsted - Acid can donate protons - Base can accept protons - There are two classes of acids** - Carbonic acid H2CO3 - Each day 15000 mmol of CO2 are generated - CO2 not acid but combines with water to form carbonic acid H2CO3 - CO2 cleared by the lungs - Noncarbonic acid - Formed from metabolism of protein. Sulfur containing AA generate H2SO4. Only 50-100 mEq of acid produced from these sources. - Cleared by the kidneys - Law of Mass Action - Velocity of reaction proportional to the product of the concentrations of the reactants - Goes through mass action formula for water - Concludes that water has H of 155 nanoM/L, more than the 40 in plasma - Says you can do the same mass experiment for every acid in the body - Can do it also for bases but he is not going to. - Acids and Bases can be strong or weak - Strong acids completely dissociate - Weak acids not so much - H2PO4 is only 80% dissociated - Weak acids are the principle buffers in the body - Then he goes through how H is measured in the blood and it becomes clear why pH is a logical way to measure. - Then there is a lot of math - HH equation - Derives it - Then uses it to look at phos. Very interesting application - Buffers - Goes tot he phosphate well again. Amazing math describing how powerful buffers can be - Big picture the closer the pKa is to the starting pH the better buffer, i.e. it can absorb lots of OH or H without appreciably changing pH - HCO3 CO2 system - H2CO3 to H + HCO3 has a PKA of 2.72 but then lots of Math and the bicarb buffer system has a pKa of 6.1 - But the real power of the bicarb buffer is that it is not a sealed system. The ability to ventilate and keep CO2 constant increases the buffering efficiency by 11 fold and the ability to lower the CO2 below normal increases 18 fold. - Isohydric principle - There is only one hydrogen ion concentration and since that is a critical part of the buffer equation, all buffer eq are linked and you can understand all of them by understanding one of them. So we just can look at bicarb and understand the totality of acid base. - Bicarb is the most important buffer because - High concentration in plasma - Ability for CO2 to ventilate - Other buffers include - Bone - Bone is more than just inorganic reaction - Live bone releases more calcium in response to an acid load than dead bone - More effect with metabolic acidosis than respiratory acidosis - Hgb - Phosphate - Protein

V tokratnem Gymnasiumu pa o knjigi slovenske uporniške poezije in albumu H2SO4 ene najbolj prepoznavnih ustvarjalk slovenske hip hop in rap scene - ankaranske glasbenice Masayah, ki je prišla v studio Prvega v družbi dr. Igorja Sakside. Avtorica in voditeljica oddaje je Liana BuršičEna najbolj prepoznavnih ustvarjalk slovenske hip hop in rap scene v družbi velikanov slovenske poezije ft. dr. Igor SaksidaV tokratnem Gymnasiumu pa o knjigi, ki je pred kratkim izšla pri založbi Beletrina in prinaša izbor pesmi upora velikanov in velikank slovenske poezije ter tematske premisleke 34-ih sodobnikov z različnih področij ustvarjanja, ki s svojim delom izstopajo iz okvirja povprečnosti. Zapisi pričajo o globinski moči poezije in pomenu upora ter svobode. Antologija pa vsebuje tudi 8 besedil z albuma ene naših najbolj prepoznavnih in ustvarjalno izstopajočih glasbenic - hiphoparke in raperke Masayah, Ankarančanke Mie Puhar Rodin.  Knjiga vsebuje tudi QR kodo s katero lahko dostopate do njenega albumskega prvenca H2SO4, knjiga pa vsebuje tudi fotografije, grafite, ilustracije in je pravzaprav celostna umetnina. Njen pobudnik in soavtor je zgodovinar dr. Igor Saksida, ki se je Masayah in oboževalcema njenega ustvarjanja Juretu Klobčarju in Jaši Mahniču,  pridružil v studiu Prvega za debato z voditeljico Liano Buršič. O globinski moči poezije, smiselnosti kletvic, pomenu upora in svobode ter povezovanja skupnosti.

Masayah je karizmatična unikatna bomba, ki izstopa od uveljavljenih trendov glasbene industrije - besedila si piše sama, trendom se ne prilagaja, vsebine ne olepšuje in pravi, da je itak buraz! Svobodni duh izraža kot raperka, pevka, kitaristka, poetinja (pa še ful stvari). Pogovarjali sva se o razliki med Mio in Masayo, o tem, kako je bit ženska na slovenski hip hop sceni, kako je zašarmirala prvo bejbo in zbežala od doma, o izgubi očeta in o tem, kaj zanjo pomeni upor. Pa seveda o njenem prvem albumu in zbirki slovenske uporniške poezije - H2SO4. Zapiski: Masayah na InstagramuMasayah na YouTubeZbirka slovenske uporniške poezije H2SO4H2SO4 koncert v Križankah   Katja je na instagramu doma tukaj.

Physics aur Chemistry badi bewafa.. raat bhar rato... Subah Safaa! Physics-Chemistry jaise bhari bharkam subjects ke sath agar aapne ishq ka subject bhi choose kar liya na ... Toh result aane par apke jeevan ke saath apki chemistry pe concentrated H2SO4 ka Chhalaa pad sakta hai.. Shayad Amir Khan ko jaldi samjh agaya tha, Isliye unhone graduate hone ke liye chuni "ARTS SIDE". O teri !! Arey Dangal wale Amir nahi Janaab... Kahaniyon Ka Mantra mein aaj ki kahani ke Amir Khan!

Investigating potential phototrophy, habitability, and bioengineering of microbes and potential floating algae in the lower, middle, and upper cloud layers of Venus with our guest, Rakesh Mogul, Ph.D., Professor of Biological Chemistry and Director; NASA/CSU Spaceward Bound, California State Polytechnic University, Pomona. Professor Rakesh recently published a study outlined below in finding that sunlight filtering through Venus' clouds could support Earth-like photosynthesis round-the-clock in Venus' clouds with the middle and lower clouds receiving similar solar energy as Earth's surface. Mogul R, Limaye SS, Lee YJ, Pasillas M. Potential for Phototrophy in Venus' Clouds. Astrobiology. October, 2021;21(10):1237-1249. https://doi.org/10.1089/ast.2021.0032 Professor Rakesh's Website: https://www.cpp.edu/~rmogul/home.html Discussion/topics include: Part 1: Phototrophy and Habitability in Venus Clouds Bacterial chlorophyll B, floating algal blooms, cloud chemistry, photophysical/chemical/biological habitability, hammett acidity factor, bioavailable water activity level, neutralized sulfuric acid favor a habitable zone, solar irradiances for photosynthesis, primary biological aerosol particles (PBAP), NASA 1kg Aircraft Bioaerosol Collector (ABC), airborne microbial metabolism and spores up to 38km in Earth's clouds, mitosis cell division in clouds Part 2: Bioengineering Investigating how to apply the following systems to adapt microbial life to local conditions in Venus clouds: Venus sulfuric acid (H2SO4) coatings, airborne DNA sequencers, Bioengineering Whispering gallery mode (WGM) phycobilliproteins, biophotonic Optofluidic Microcavities Liquid Crystal Droplets, introducing an enzyme into the water to increase H production by 400%, UV resistant nanostructured coatings and biofouling hydrophilic coatings, self replicating algae mats and floating algae ISRU bioreactors in clouds of Venus --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app Support this podcast: https://anchor.fm/frontierspace/support

Podcast episode 23 is up today on the LMNT electrolytes, and asking the question, What do electrolytes have to do with the gut? Here's the episode with the one and only Robb Wolf.Robb Wolf, is a former research biochemist and 2X New York Times/Wall Street Journal Best-selling author of The Paleo Solution and Wired To Eat.He and co-author Diana Rodgers recently released their book, Sacred Cow, which explains why well-raised meat is good for us and good for the planet.Robb has transformed the lives of hundreds of thousands of people around the world via his top-ranked Itunes podcast, books and seminars.He's known for his direct approach and ability to distill and synthesize information to make the complicated stuff easier to understand.Robb is also the co-founder of Drink LMNT.I drink LMNT everyday to support intermittent fasting, my workouts, and optimal digestion. My favorite flavor can be found below!GET YOUR FREE DRINK LMNT SAMPLE PACKLMNT Electrolytes (What do Electrolytes Have to Do with the Gut?)Click HERE to save this post for later.Resources MentionedWired to EatLMNTRobb on InstagramRobb's personal websiteSacred CowThe Paleo SolutionDon't Miss These ThoughtsRobb's storyHis diet then and todayThe gut from a biochemical standpointWhat exactly are electrolytes and why are they necessary for the gut?Symptoms of an electrolyte imbalanceHow and why does an electrolyte imbalance lead to digestive issues?“An electrolyte imbalance can cause gut problems and gut problems can cause an electrolyte imbalance.”What does leaky gut have to do with all of this?How Robb founded LMNTWhat is the natriuresis of fasting?Robb's personal favorite LMNT flavor (get it HERE)Something about electrolytes most people get wrongRobb's 3 convictions around gut health and gut healingMore from A Gutsy Girl1. Welcome to A Gutsy Girl Podcast2. Hang out on Instagram3. BFF's on YouTube4. Free resource: The Master Gutsy Spreadsheet5. Rated-G Email ClubLMNTHere is more information on the LMNT product:LMNT is a tasty electrolyte drink mix with everything you need and nothing you don't. That means lots of salt — with no sugar. LMNT is formulated to help anyone with their electrolyte needs and is perfectly suited to folks following a keto, low-carb, or paleo diet. With none of the junk. No sugar, coloring, artificial ingredients, gluten, or fillers.Current flavors include:Watermelon SaltCitrus SaltOrange SaltRaspberry SaltRaw UnflavoredMango ChiliLemon HabaneroChocolate SaltMint Chocolate (BRAND NEW!)GET YOUR FREE DRINK LMNT SAMPLE PACKStrong ElectrolytesHere are 4 main and common strong electrolytes:HCl (hydrochloric acid)H2SO4 (sulfuric acid)NaOH (sodium hydroxide)KOH (potassium hydroxide)And according to one source, here is the digestive benefit: Electrolytes keep the digestive system chugging along. Your intestines are lined with smooth muscle tissue that's controlled by the autonomic nervous system, the part you can't consciously control. Their rhythmic contractions are important for nutrient absorption and waste elimination. Potassium allows the muscles in the intestines to contract. However, low potassium levels can inhibit healthy digestion. That's why it's so important to load up on potassium with food and electrolyte supplements! But it's more than just that from a digestive standpoint. Keep reading to learn more about why electrolytes are critical for the Gutsy community.Sources: HERE, and HEREHow to Get ElectrolytesSome of the main causes of electrolyte imbalance include dehydration, sweating, diarrhea, certain medications, and vomiting.Because these are all very common in the Gutsy community, you can understand the chicken/egg scenario Robb discusses in the episode.So how can you get more electrolytes?For me and in/because of my research, supplementing is quickest and best for electrolytes. This is why, the electrolytes powder packets from LMNT are powerful.Electrolytes Powder PacketsI have the best electrolytes powder packets to share.In fact, I included these on my Holiday 2021 Wish List.However, today my favorite flavor releases and I can't even stand how excited I am about it.The flavor? Mint Chocolate. I'm a sucker for Mint Chocolate always, and this one is fantastic!It contains:1,000 mg sodium200 mg potassium60 mg magnesiumI got a sneak preview of the flavor and have been drinking it for the past couple weeks. So let me share a couple things.How to drink a packet of LMNTThe first time I tried LMNT I made a huge mistake. I poured an entire packet (stick) into about 8-10 ounces of water. Literally gagged and was like, “I cannot talk about this product because it tastes like colonoscopy prep.” Ladies – you know I'm always real and honest with you. That's what I thought.Well then I actually read the usage instructions and had the conversation with Robb. Turns out that if you drink an entire stick with just 8 – 10 ounces, it's going to be salty AF.So don't do as I did.Instead, for best results and the most incredible taste, pour the stick into 30 – 32 ounces and stir. I promise it tastes so good. Like, so good I now need to make sure I'm only drinking 1 – 2 sticks per day (or as needed with workouts!)I personally love the Mint Chocolate flavor over water and ice (was thinking of blending it next?!?!).Anyways, that's all you do to reap the benefits.I'M READY TO GET MY FREE LMNT SAMPLE PACKElectrolytes Supplement KetoOne final thing I have to mention: the Keto community loves this product.And if you're part of the Keto community, surely you have felt the “keto flu.”The body excretes electrolytes at an increased rate due while in a low-carb, ketogenic, or fasted state. Similar to the low-carb flu, electrolytes can make the difference between feeling great and feeling like garbage on a fast.I'll tell you what's real – I started drinking this and felt better before, during, and after my workouts. I also consumed a whole stick a night after having one too many cocktails and it did some magic!Finally, this product does use Stevia and I've always been skeptical of how my body (aka acne) reacts with Stevia. I'm keeping my eye on it with the handy, dandy, super lovely healing journal I created. You can, too! Wrap UpTime to wrap this up. As always, a huge goal for this show is to connect with even more people. Feel free to send an email to our team at podcast@agutsygirl.com. We want to hear questions, comments, show ideas, etc.Did you enjoy this episode? Please drop a comment below or leave a review on Apple Podcasts.Xox,SKH Connect with A Gutsy GirlThrough the websiteOn InstagramVia LinkedIn

Podcast episode 23 is up today on the LMNT electrolytes, and asking the question,What do electrolytes have to do with the gut?Here's the episode with the one and only Robb Wolf.Robb Wolf, is a former research biochemist and 2X New York Times/Wall Street Journal Best-selling author of The Paleo Solution and Wired To Eat.He and co-author Diana Rodgers recently released their book, Sacred Cow, which explains why well-raised meat is good for us and good for the planet.Robb has transformed the lives of hundreds of thousands of people around the world via his top-ranked Itunes podcast, books and seminars.He's known for his direct approach and ability to distill and synthesize information to make the complicated stuff easier to understand.Robb is also the co-founder of Drink LMNT.I drink LMNT everyday to support intermittent fasting, my workouts, and optimal digestion. My favorite flavor can be found below!GET YOUR FREE DRINK LMNT SAMPLE PACKLMNT Electrolytes (What do Electrolytes Have to Do with the Gut?)Click HERE to save this post for later.Resources MentionedWired to EatLMNTRobb on InstagramRobb's personal websiteSacred CowThe Paleo SolutionDon't Miss These ThoughtsRobb's storyHis diet then and todayThe gut from a biochemical standpointWhat exactly are electrolytes and why are they necessary for the gut?Symptoms of an electrolyte imbalanceHow and why does an electrolyte imbalance lead to digestive issues?“An electrolyte imbalance can cause gut problems and gut problems can cause an electrolyte imbalance.”What does leaky gut have to do with all of this?How Robb founded LMNTWhat is the natriuresis of fasting?Robb's personal favorite LMNT flavor (get it HERE)Something about electrolytes most people get wrongRobb's 3 convictions around gut health and gut healingMore from A Gutsy Girl1. Welcome to A Gutsy Girl Podcast2. Hang out on Instagram3. BFF's on YouTube4. Free resource: The Master Gutsy Spreadsheet5. Rated-G Email ClubLMNTHere is more information on the LMNT product:LMNT is a tasty electrolyte drink mix with everything you need and nothing you don't. That means lots of salt — with no sugar.  LMNT is formulated to help anyone with their electrolyte needs and is perfectly suited to folks following a keto, low-carb, or paleo diet. With none of the junk. No sugar, coloring, artificial ingredients, gluten, or fillers.Current flavors include:Watermelon SaltCitrus SaltOrange SaltRaspberry SaltRaw UnflavoredMango ChiliLemon HabaneroChocolate SaltMint Chocolate (BRAND NEW!)GET YOUR FREE DRINK LMNT SAMPLE PACKStrong ElectrolytesHere are 4 main and common strong electrolytes:HCl (hydrochloric acid)H2SO4 (sulfuric acid)NaOH (sodium hydroxide)KOH (potassium hydroxide)And according to one source, here is the digestive benefit:Electrolytes keep the digestive system chugging along. Your intestines are lined with smooth muscle tissue that's controlled by the autonomic nervous system, the part you can't consciously control. Their rhythmic contractions are important for nutrient absorption and waste elimination. Potassium allows the muscles in the intestines to contract. However, low potassium levels can inhibit healthy digestion. That's why it's so important to load up on potassium with food and electrolyte supplements!But it's more than just that from a digestive standpoint. Keep reading to learn more about why electrolytes are critical for the Gutsy community.Sources: HERE, and HEREHow to Get ElectrolytesSome of the main causes of electrolyte imbalance include dehydration, sweating, diarrhea, certain medications, and vomiting.Because these are all very common in the Gutsy community, you can understand the chicken/egg scenario Robb discusses in the episode.So how can you get more electrolytes?For me and in/because of my research, supplementing is quickest and best for electrolytes. This is why, the electrolytes powder packets from LMNT are powerful.Electrolytes Powder PacketsI have the best electrolytes powder packets to share.In fact, I included these on my Holiday 2021 Wish List.However, today my favorite flavor releases and I can't even stand how excited I am about it.The flavor? Mint Chocolate. I'm a sucker for Mint Chocolate always, and this one is fantastic!It contains:1,000 mg sodium200 mg potassium60 mg magnesiumI got a sneak preview of the flavor and have been drinking it for the past couple weeks. So let me share a couple things.How to drink a packet of LMNTThe first time I tried LMNT I made a huge mistake. I poured an entire packet (stick) into about 8-10 ounces of water. Literally gagged and was like, “I cannot talk about this product because it tastes like colonoscopy prep.” Ladies – you know I'm always real and honest with you. That's what I thought.Well then I actually read the usage instructions and had the conversation with Robb. Turns out that if you drink an entire stick with just 8 – 10 ounces, it's going to be salty AF.So don't do as I did.Instead, for best results and the most incredible taste, pour the stick into 30 – 32 ounces and stir. I promise it tastes so good. Like, so good I now need to make sure I'm only drinking 1 – 2 sticks per day (or as needed with workouts!)I personally love the Mint Chocolate flavor over water and ice (was thinking of blending it next?!?!).Anyways, that's all you do to reap the benefits.I'M READY TO GET MY FREE LMNT SAMPLE PACKElectrolytes Supplement KetoOne final thing I have to mention: the Keto community loves this product.And if you're part of the Keto community, surely you have felt the “keto flu.”The body excretes electrolytes at an increased rate due while in a low-carb, ketogenic, or fasted state. Similar to the low-carb flu, electrolytes can make the difference between feeling great and feeling like garbage on a fast.I'll tell you what's real – I started drinking this and felt better before, during, and after my workouts. I also consumed a whole stick a night after having one too many cocktails and it did some magic!Finally, this product does use Stevia and I've always been skeptical of how my body (aka acne) reacts with Stevia. I'm keeping my eye on it with the handy, dandy, super lovely healing journal I created. You can, too! Wrap UpTime to wrap this up. As always, a huge goal for this show is to connect with even more people. Feel free to send an email to our team at podcast@agutsygirl.com. We want to hear questions, comments, show ideas, etc.Did you enjoy this episode? Please drop a comment below or leave a review on Apple Podcasts.Xox,SKH

00:00 - Intro01:33 - We're in an muriatic acid shortage. Thanks, COVID.02:21 - Two specialty acids: modified Muriatic Acids for less fuming: AcidBlue and AcidMagic. 03:06 - Muriatic acid is a diluted form of Hydrochloric acid (HCl). It is 31.45% HCl or less.04:14 - Sulfuric acid (H2SO4) is sold in 38.5% concentration. It is comparable in dosing to standard 31.45% HCl. It takes just 2% more sulfuric acid to equal muriatic by volume.09:36 - Sodium bisulfate (NaHSO4) is sold in 93.2% concentration. It is also known as "dry acid", or in pool retail stores, "pH down" or "alkalinity down". It is safer to handle than liquid acid, but needs to be pre-dissolved before adding to the pool.11:48 - Let's talk about sulfates (SO4--) or (SO3--).12:05 - One gallon of 38.5% sulfuric acid leaves behind 47.1 ppm of sulfates in 10,000 gallons.13:19 - One pound of 93.2% of sodium bisulfate leaves behind 9.6 ppm of sulfates in 10,000 gallons, plus salt.14:58 - even in perfectly LSI-balanced water, if you have high enough sulfates, you can still have etching of cement. The sulfate ion (SO3--) can become the dominant ion and kicks carbonate off of calcium (Ca++) and create calcium sulfate.  Enough calcium sulfate can precipitate a sharp crystalline scale.18:08 - The only way to reduce sulfates is to drain and dilute.  Unless you have Reverse Osmosis (R.O.) available. If you're going to use sulfuric or sodium bisulfate, you must regularly schedule dilutions to avoid sulfate problems.19:53 - Sulfates and metals can combine to create that infamous 'rotten egg' smell. We think of it as sulfur, but it's usually iron sulfate or some variant.21:08 - The third alternative for pH reduction is injecting carbon dioxide (CO2). It reduces pH but does not reduce alkalinity. In fact, alkalinity tends to rise due to excess lye from chlorine.22:18 - Acid only introduces more CO2 (to reduce pH) is to burn through alkalinity and convert it into carbonic acid.  And Joe thought I was asking a trick question. There is no CO2 in acid.24:39 - One pound of CO2 is equivalent to 32.8 fl.oz. of standard Muriatic Acid for pH correction.27:08 - Summary------------------------------------Connect with Orenda TechnologiesWebsite: https://www.orendatech.comBlog: https://blog.orendatech.comYouTube: https://www.youtube.com/user/OrendaTechnologiesFacebook: https://www.facebook.com/orendatech/Instagram: https://www.instagram.com/orendatechnologies/

A frontember most is vitte a showt... Első alkalommal készítettünk online video-interjút, de Marcinál ez a közeg is működik. Az epizód utolós 5 percében "COVID-19 intermezzoval" is előrukkolunk, már csak ezért is érdemes ezúttal nem csak hallgatni, végig is nézni a teljes epizódot! H2So4, a templomi csengettyűszó, a pálcikaemberbe belelátott öngyilkossági hajlam, katonanóták a szombathelyi vonaton, az okos és a bohóc szereposztás..., csupa újdonság, amit Marcitól, Marciról még nem igazán hallhattunk.

Caitlin, Anya, and Alan talk about a universe where they banged a physicist- and a universe where they didn’t. We also talk about Chapters 10-13 of The Golden Compass. We find out that John Calvin believed in boring things, that no cats were harmed in Schrödinger’s experiment, and #NotAllBears.The slur ‘Gypsy’ comes from a mutation of Egyptian. The Roma/ Sinti / Traveler people came from northern India, and not Africa.Anya’s equation for making gas from iron filings looks like this: With dilute H2SO4, you get a standard metal-acid redox reaction - Iron (II) Sulphate & hydrogen gas are the products: Fe (s) + H2SO4 (aq) → FeSO4 (aq) + H2 (g)Quantum Theory and The Uncertainty Principle are counter-intuitive, but have proven to be the most reliable mathematical model in Physics.Richard Feynman bragged about his womanizing in his loose autobiography ‘Surely You’re Joking Mr Feynman’. He often complains that women won’t give him the sex he wants, so what is the point in being polite to them?It is unclear who said, "Anyone who claims to understand quantum theory is either lying or crazy,” but it is often attributed to Feynman.What is Schrödinger's Cat?What is the Many-Worlds Interpretation of Quantum Mechanics?What is the Many-Worlds version of String Theory?The Multiverse TropeDeepak Chopra melds counter-intuitive science with mysticism, and sells a lot of books.The last thing Stephen Hawking wrote was “A Smooth Exit from Eternal Inflation?” which set a limit on the number of possible universes.What are the Northern Lights?Witches?John Calvin believed in the total sovereignty of God.Wait. The Puritans were real?A concise explanation of Calvin’s view on “Free Will”.Cartesian Dualism is a thing.Does a body need a mind to exist?Nature vs NurtureCanadian Geese are trigger-happy attack-dogs with wings.Beowulf was a were-bearTexas was its own countryWhat is a Zorro?Read Chapters 14-17 for next time!!Our theme song is Clockwork Conundrum by NathanGunnFollow us on Twitter: Anya @StrangelyLiterl Cailtlin @inferiorcaitlin The Podcast @MoTPodPlease email us contact@hallowedgroundmedia.com

In this episode, we talk about what Gandalf and his knowledge of the One Ring. Why doesn’t Gandalf know right away that Bilbo has Sauron’s ring? How did he figure it out? How did the ring get to a place where Gollum could find it? We talk about the dwarven rings, the One Ring’s effects on mortals, the Council of Elrond, the public library system of Gondor, and what would happen if Gandalf put on the One Ring while wearing the elvish ring that he already has. Short answer: it would be bad. In other news, Dan makes fun of Peter Jackson. 1:05 - Bilbo finding the ring - Riddle party! 3:35 - How does Gandalf not know it’s the One? 4:48 - Dwarf boats are barrels 5:12 - Back to Gandalf not knowing if it’s the One ring or not... 5:30 - Rings granting invisibility 5:43 - Greater/lesser rings 6:00 - I said Eregon. I meant Eregion. Those are different things. I blame the rye. -Erica 6:35 - How did the ring get here? 7:09 - Isildur’s bane 7:54 - Hobbit susceptibility to rings 8:07 -  Dwarf rings 8:20 - I said that Sauron didn’t know about the 3 elven rings. He actually knows about all of them, but he doesn’t know where they are. The people that have the elf rings can use them, but the more dramatic the use, the more noticeable they make themselves. When the fellowship is crossing Caradhras, Gandalf uses the power of his ring to start a fire. He mentions that everyone knows exactly where he is when he does it. - Erica 8:40 - Back to the Dwarves - Gold! Madness! 9:00 - Dan is making fun of Peter Jackson. 10:00 - Thorin’s family, gold sickness, and the dwarf rings 10:53 - Why does Sauron want the dwarf rings? 11:15 - Dain putting the Mouth of Sauron on hold / Council of Elrond 12:15 - The fireplace at Bag End 12:30 - Effects of rings on mortals 12:51 - One ring is for enslaving others - Bilbo wants to live in peace and plant potatoes and dream #Moomin 13:10  - #notallhobbits 13:42 - Erica fangirls over Sam very briefly 14:20 - Sauron and Gollum 15:50 - Aragorn found Gollum in the Dead Marshes and was working with Gandalf 16:00 - Gollum did some bad stuff in Mirkwood, ended up prison breaking out of Thranduil's dungeon. Bilbo was able to escape from Thranduil with a baker’s dozen of dwarves in barrels and Gollum was able to get away because they let him out to climb trees. I don’t think he’s really that keen on keeping people prisoner… 17:00 - Gollum is why Legolas is at the Council of Elrond 17:20 - The gap between the party and Frodo leaving for Rivendell is 17 years 17:58 - Gandalf at Bilbo’s party - Great rings extending life (one book into three movies) 19:45 - Gandalf’s research in Minas Tirith - Erica looks at the actual book to confirm. - Isildur and the fire letters. #research #soproud 21:15 - Keep it secret, keep it safe, y’all! 21:44 - Gandalf and the big bucket of NOPE! 22:44 - Why did Gandalf know to go to minas tirith? - Minas Tirith is smart and funds their public library system to maintain the Isildur Archives #primarysources 23:25 - Frodo leaving the Shire (If Gandalf isn’t back by this time = September) - Nazgûl word problems - Saruman doesn’t care 25:37 - What if Gandalf put on the ring to be sure it’s the One? Is it like like drinking the clear liquid in the chemistry Lab? What you thought was H2O was H2SO4! 26:50 - Gandalf touches the ring in the book, but not in the movies. Artistic license! 27:37 - Sauron’s involvement in ring making 27:54 - I said Eregon again. Still meant Eregion. Erica is facepalming so hard. 28:48 - Rings and invisibility again, who turns invisible and who doesn’t? 30:40 - Sam also turned invisible 31:04 - Sauron can’t change shape because of the fall of Númenor. 31:34 - Shadow of Mordor, when Sauron is Celebrimbor’s ring coach, he looks like an elf lord (Annatar, Lord of Gifts) because it’s before the fall of Númenor 32:28 - The short version of the fall of Númenor.

In this devil may care episode number 50 of the STAB! program, John Ross welcomes Alfonso Portela, Jaclyn Weiand, Tyler Kinney and Jesse Jones for discussions of Apple Day in the UK, the Aberfan Disaster, Aroldis Chapman, John Paul Getty III, Dizzy Gillespie– not Louis Armstrong, the denouncement of lynching, National Nurse’s Day in Thailand, … Continue reading »

Matériel : trois béchers d'un litre, six béchers de 250 ml, trois béchers de 50 ml, trois bâtons de verre, éprouvette de 500 ml, horloge, lunettes et gants de protection Produits chimiques : eau distillée, KIO3, Na2SO3, amidon, H2SO4 concentré, éthanol Solution A : 8.6 g KIO3, dissout dans 200 ml d'eau Solution B : 8 g H2SO4 concentré, 20 ml d'éthanol, 2.32 g Na2SO3, dans 2000 ml d'eau Solution C : 1 g d'amidon dans 500 ml d'eau chaude. Cette solution doit être préparée juste avant l'expérience Procédure expérimentale : Eau distillée, solution C (amidon) et la solution de sulfite (B) sont placées une après l'autre dans les trois grands béchers (quantités plus loin). Après addition de la solution B les solutions sont bien remuées. La quantité nécessaire de solution A doit être mise simultanément dans les 3 béchers : Bécher 1 : 200 ml d'eau + 20 ml solution C + 100 ml solution B + 100 ml solution A Bécher 2 : 400 ml d'eau + 20 ml solution C + 100 ml solution B + 100 ml solution A Bécher 3 : 600 ml d'eau + 20 ml solution C + 100 ml solution B + 100 ml solution A Après avoir ajouté la solution A le contenu des trois béchers est bien remué, puis laissé pour env. 7 secondes. Le changement de couleur vers le bleu apparaît dans le premier bécher après 10 à 15 secondes, dans le 2e après env. 30 secondes, et dans le 3e après 1 minute. Une grande horloge est pratique pour relever ces temps. Explication : trois réaction sont impliquées, dont la première, lente, détermine le changement de couleur. Les ions iodate IO3– sont réduits par les hydrogène-sulfites en iodures IO3– + HSO3– → I– + 3 HSO4– (lent) Les iodures sont rapidement consommés par médiamutation pour donner de l’iode élémentaire, qui réagit avec l'amidon pour former un complexe de couleur bleue : IO3– + 5 I– + 6 H+ → 3 I2 + 3 H2O (rapide, donnant la « couleur bleue ») Tant qu'il reste des ions hydrogène sulfite, le complexe avec l'amidon n'est pas stable I2 + HSO3– → 2 I– + HSO4– + H3O+ (très rapide, consommant la « couleur bleue ») Pour que le bleu du complexe iode-amidon persiste, tous les ions hydrogène sulfite doivent être consommés. Elimination des déchets : les solutions sont inoffensives, de faible concentration, et peuvent passer par l'évier. H.W. Roesky et W. Möckel, « Chemical Curiosities », page 270, 1996, Copyright Wiley-VCH Verlag GmbH and Co. KGaA. Traduit de l'anglais avec permission.

Mesures de sécurité : port de lunettes de protection obligatoire Matériel : électrolyseur (grande éprouvette avec connecteur et bouchon avec 2 électrodes en nickel, avec support, transformateur, robinet à gaz), petite assiette en porcelaine, pique en bois (env. 30 cm) Produits chimiques : H2SO4 à 1 mol/L, solution de savon Procédure expérimentale : un mélange d'oxygène et d'hydrogène est produit par électrolyse de la solution de H2SO4, par une tension de 20 Volt. Le mélange est conduit dans la solution de savon, pour la faire mousser. Le courant est coupé, et l'assiette porté à au moins un mètre de l'électrolyseur, puis le gaz allumé avec le pique incandescent. Le mélange explose avec un grand fracas pour produire de l'eau. L'explosion peut être si violente que l'assiette ne résiste parfois pas. Il faut absolument s'assurer de la distance suffisante entre l'électrolyseur et le lieu de l'explosion, sinon le générateur de gaz risque d'exploser, projetant des éclats de verre et d'acide. H.W. Roesky et W. Möckel, « Chemical Curiosities », page 287, 1996, Copyright Wiley-VCH Verlag GmbH and Co. KGaA. Traduit de l'anglais avec permission.

Matériel : bécher de 500 ml, trois béchers de 200 ml, agitateur magnétique avec aimant, lunettes et gants de protection Produits chimiques : acide malonique HOOCCH2COOH, iodate de sodium NaIO3, MnSO4 x H2O, H2SO4 à 1 mol/L, H2O2 à 10 %, amidon soluble, eau distillée Procédure expérimentale : trois solutions sont préparées Solution A : 1.5 g d'iodate de sodium et 10 ml H2SO4 à 1 mol/L avec 100 ml d'eau distillé Solution B : 1 g d'acide malonique, 1.5 g sulfate de manganèse et 10 ml d'une solution d'amidon à 1 % avec 100 ml d'eau distillé Solution C : 135 ml d'eau oxygéné à 10 % Les trois solutions incolores sont versées simultanément dans le grand bécher et bien agitées. Après un petit moment l'oscillation entre une couleur bleue et légèrement jaune démarre. Explication : le réaction de Belousov-Zhabiotinsky utilisée ici est initiée par la réduction du iodate en iode élémentaire par l'acide malonique et le sulfate de Mn. Le présence du iode élémentaire est mise en évidence par la formation du complexe iode/amidon de couleur bleu intense. Le iode élémentaire réagit ensuite avec l'acide pour donner de l'acide mono ou di-substitué en iode transparent. La réaction se termine par une complexion lente des ions Mn(II) par l'acide malonique substitué. Elimination des déchets : le volume, traité avec une solution de lait de chaux, est décanté, puis les résidus insolubles sont transférés dans un bidon pour sels inorganiques de faible toxicité. La solution, à pH 7 à 8, est inoffensive et peut passer à l'évier. H.W. Roesky et W. Möckel, « Chemical Curiosities », page 264, 1996, Copyright Wiley-VCH Verlag GmbH and Co. KGaA. Traduit de l'anglais avec permission.

In this activity, the effects that varying pH levels have on plants are tested as a way to see the importance of clean, fresh water to living things. This activity will also demonstrate that water pollution is not just a local issue, but rather a global issue. Explanation: Acid rain is a prime example of how activities in one area can have a serious effect on conditions of a global scale. Acid rain primarily results from the transformation of industrial pollutants such as sulphur dioxide (SO2) and nitrogen oxides into other compounds such as sulphuric acid (H2SO4), and nitric acid (HNO3). This transformation occurs as these pollutants are transported in the atmosphere over distances of hundreds to thousands of kilometers. For example, sulfur dioxide emissions from industrial processes and the burning of fossil fuels have resulted in extensive acid rain and accompanying water pollution problems in southeastern Canada and the northeastern US. These emissions have global implications: more than half of the acid deposition in eastern Canada originates from emissions in the United States. Even slight changes in the pH of lakes and rivers can cause the loss of fish and invertebrates which are important links in the food chain. Acid rain is also responsible for extensive loss of forest cover in that region.

Good yields of tertiary alkanoic acids are obtained from the Koch-Haaf-synthesis even when only stoichiometric amounts of carbinol and HCOOH are used. This offers a new approach to 13CO-labelled tertiary alkanoic acids. - An excess of HCOOH is generally used in the Koch-Haaf-synthesis1) of carboxylic acids from carbinols and HCOOH in conc. H2SO4.