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Which Metabolic Rate Resulted In Metabolic Acidosis?

Glutamine Metabolism: Role In Acid-base Balance*

Glutamine Metabolism: Role In Acid-base Balance*

Abstract The intent of this review is to provide a broad overview of the interorgan metabolism of glutamine and to discuss in more detail its role in acid-base balance. Muscle, adipose tissue, and the lungs are the primary sites of glutamine synthesis and release. During normal acid-base balance, the small intestine and the liver are the major sites of glutamine utilization. The periportal hepatocytes catabolize glutamine and convert ammonium and bicarbonate ions to urea. In contrast, the perivenous hepatocytes are capable of synthesizing glutamine. During metabolic acidosis, the kidney becomes the major site of glutamine extraction and catabolism. This process generates ammonium ions that are excreted in the urine to facilitate the excretion of acids and bicarbonate ions that are transported to the blood to partially compensate the acidosis. The increased renal extraction of glutamine is balanced by an increased release from muscle and liver and by a decreased utilization in the intestine. During chronic acidosis, this adaptation is sustained, in part, by increased renal expression of genes that encode various transport proteins and key enzymes of glutamine metabolism. The increased levels of phosphoenolpyruvate carboxykinase result from increased transcription, while the increase in glutaminase and glutamate dehydrogenase activities result from stabilization of their respective mRNAs. Where feasible, this review draws upon data obtained from studies in humans. Studies conducted in model animals are discussed where available data from humans is either lacking or not firmly established. Because there are quantitative differences in tissue utilization and synthesis of glutamine in different mammals, the review will focus more on common principles than on quantification. Continue reading >>

Disorders Of Acid-base Balance

Disorders Of Acid-base Balance

Metabolic Acidosis: Primary Bicarbonate Deficiency Metabolic acidosis occurs when the blood is too acidic (pH below 7.35) due to too little bicarbonate, a condition called primary bicarbonate deficiency. At the normal pH of 7.40, the ratio of bicarbonate to carbonic acid buffer is 20:1. If a person’s blood pH drops below 7.35, then he or she is in metabolic acidosis. The most common cause of metabolic acidosis is the presence of organic acids or excessive ketones in the blood. [link] lists some other causes of metabolic acidosis. *Acid metabolites from ingested chemical. Common Causes of Metabolic Acidosis and Blood Metabolites Cause Metabolite Diarrhea Bicarbonate Uremia Phosphoric, sulfuric, and lactic acids Diabetic ketoacidosis Increased ketones Strenuous exercise Lactic acid Methanol Formic acid* Paraldehyde β-Hydroxybutyric acid* Isopropanol Propionic acid* Ethylene glycol Glycolic acid, and some oxalic and formic acids* Salicylate/aspirin Sulfasalicylic acid (SSA)* The first three of the eight causes of metabolic acidosis listed are medical (or unusual physiological) conditions. Strenuous exercise can cause temporary metabolic acidosis due to the production of lactic acid. The last five causes result from the ingestion of specific substances. The active form of aspirin is its metabolite, sulfasalicylic acid. An overdose of aspirin causes acidosis due to the acidity of this metabolite. Metabolic acidosis can also result from uremia, which is the retention of urea and uric acid. Metabolic acidosis can also arise from diabetic ketoacidosis, wherein an excess of ketones is present in the blood. Other causes of metabolic acidosis are a decrease in the excretion of hydrogen ions, which inhibits the conservation of bicarbonate ions, and excessive loss of bicarbonate Continue reading >>

Blood Gas Analysis--insight Into The Acid-base Status Of The Patient

Blood Gas Analysis--insight Into The Acid-base Status Of The Patient

Acid-Base Physiology Buffers H+ A- HCO3- CO2 Buffers H+ A- CO2 Cells Blood Kidney Lungs Fluids, Electrolytes, and Acid-Base Status in Critical Illness Blood Gas Analysis--Insight into the Acid-Base status of the Patient The blood gas consists of pH-negative log of the Hydrogen ion concentration: -log[H+]. (also, pH=pK+log [HCO3]/ 0.03 x pCO2). The pH is always a product of two components, respiratory and metabolic, and the metabolic component is judged, calculated, or computed by allowing for the effect of the pCO2, ie, any change in the pH unexplained by the pCO2 indicates a metabolic abnormality. CO +H 0ºº H CO ººHCO + H2 2 2 3 3 - + CO2 and water form carbonic acid or H2CO3, which is in equilibrium with bicarbonate (HCO3-)and hydrogen ions (H+). A change in the concentration of the reactants on either side of the equation affects the subsequent direction of the reaction. For example, an increase in CO2 will result in increased carbonic acid formation (H2CO3) which leads to an increase in both HCO3- and H+ (\pH). Normally, at pH 7.4, a ratio of one part carbonic acid to twenty parts bicarbonate is present in the extracellular fluid [HCO3-/H2CO3]=20. A change in the ratio will affect the pH of the fluid. If both components change (ie, with chronic compensation), the pH may be normal, but the other components will not. pCO -partial pressure of carbon dioxide. Hypoventilation or hyperventilation (ie, minute2 ventilation--tidal volume x respitatory rate--imperfectly matched to physiologic demands) will lead to elevation or depression, respectively, in the pCO2. V/Q (ventilation/perfusion) mismatch does not usually lead to abnormalities in PCO2 because of the linear nature of the CO2 elimination curve (ie, good lung units can make up for bad lung units). Diffus Continue reading >>

Bicarbonate

Bicarbonate

Bicarbonate is the major extracellular buffer in the body. It is present in all body fluids and can be generated from CO2 and H2O in the presence of carbonic anhydrase. Bicarbonate on the chemistry panel gives an indication of acid-base status, but does not replace blood gas measurement as it does not supply information about the respiratory component of acid-base status or the pH of the animal. Bicarbonate values on a chemistry panel should always be interpreted with the anion gap, which is a calculated result, and the corrected chloride. The anion gap and corrected chloride provides useful information for delineating causes of metabolic acidosis (loss or titration of bicarbonate) and can give you an indication of a mixed acid-base disturbance. Note, that this page refers to bicarbonate measurement with the chemistry analyzer and not a blood gas analyzer. For the latter, refer to laboratory detection page. Method of measurement The following method is used at Cornell University to measure bicarbonate on our automated chemistry analyzer. Bicarbonate can also be measured on the blood gas analyzer, which uses ion selective electrodes (and calculates bicarbonate from pH and hydrogen concentration). Reaction type Blanked end-point reaction Procedure This is a two step reaction that starts with phosphoenolpyruvate carboxylase (PEPC) catalyzing the oxidation of phosphoenolpyruvate (PEP) to oxaloacetate, in the presence of HCO3–. This first reaction is coupled to a second reaction that involves the transfer of a H+ from an nicotinamide adenine dinucleotide (NADH) analog to oxaloacetate using malate dehydrogenase (MDH). The lowered levels of NADH analog causes an absorbance decrease at 415 nm, which directly correlates to the concentration of HCO3– in the sample. The reacti Continue reading >>

Exercise 47: Acid-base Balance: Computer Simulation

Exercise 47: Acid-base Balance: Computer Simulation

4. ACTIVITY 2: HYPERVENTILATION WHAT ACID-BASE IMBALANCE OCCURRED WITH HYPERVENTILATION? THE pH VALUE BEGAN TO EXCEED THE NORMAL RANGE BETWEEN 10 AND 20 SECONDS - AS SOON AS IT ROSE ABOVE 7.45, THIS INDICATED THE CONDITION OF ALKALOSIS. 8. ACTIVITY 3: REBREATHING DID REBREATHING RESULT IN ACIDOSIS OT ALKALOSIS? WHY? HINT: SPECIFICALLY RELATE THIS TO THE LEVEL OF CO2. REBREATHING RESULTED IN ACIDOSIS BECAUSE THE pH VALUE BEGAN TO DIP BELOW THE NORMAL RANGE BETWEEN 20 AND 30 SECONDS - SOON AS IT WENT BELOW 7.35. ACIDOSIS IS THE RESULT OF IMPAIRED RESPIRATION (HYPOVENTILATION) THAT LEADS TO THE ACCUMULATION OF TOO MUCH CARBON DIOXIDE IN THE BLOOD. Continue reading >>

The Effects Of Acute Total Asphyxia And Metabolic Acidosis On Cerebrospinal Fluid

The Effects Of Acute Total Asphyxia And Metabolic Acidosis On Cerebrospinal Fluid

Pediatr. Res., 14: 286-290 (1980) acid-base balance cerebrospinal fluid asphyxia metabolic acidosis Bicarbonate Regulation in Newborn Puppies EUGENE E. NATTIE"'' AND WILLIAM H. EDWARDS Departments of Maternal and Child Health and Physiology, Dartmouth Medical School, Hanover, New Ifampshire, USA Summary We evaluated CSF [HCO;] regulation in lightly anesthetized newborn puppies following: (1) acute total asphyxiq (2) metabolic acidosis; and (3) metabolic acidosis induced after acute asphyxia. Five and one-half min of total asphyxia resulted in a 4.4 mM/liter decrease in mean CSF [HCO;]. During 65 min of recovery with mechanical ventilation mean CSF [HCOJ] increased 1.7 mM/ liter. Mean plasma [HCO;] decreased 7 mM/liter and recovered 4.5 mM/liter in the same period. We produced a stable metabolic acidosic for 4 hr using a peritoneal dialysis technique with PaCOs maintained at the normal value. With acidosis in nonaspbyxiated control puppies, CSF [HCOSl decreased steadily. At 4 hr, the ratio, ACSF [HCOSl/Aplasma [HCO;], was 0.43, a value close to that observed in adults of many species with metabolic acid- base disturbances, 0.41. With acidosis in asphyxiated puppies allowed 1 hr of recovery, the time course and mean values of plasma and CSF [HCO;] were indistinguishable from those of the nonasphyxiated acidotic controls. Newborn puppies appear to regulate CSF [HCOJl in response to acute asphyxia or metabolic acidosis, and acute asphyxia does not impair the puppy's ability to regulate CSF [HCOsl in metabolic acidosis. two wk before the estimated date of delivery. The dogs were fed Purina dog chow and water ad libitum. Following normal spon- taneous birth, puppies were at least one hr and no more than 4 days of age at the time of experiment. The general design included 4 gr Continue reading >>

4 Which Type Of Breathing Resulted In P Co2 Levels

4 Which Type Of Breathing Resulted In P Co2 Levels

Unformatted text preview: 4. Which type of breathing resulted in P CO2 levels closest to the ones we experimented with in this activity normal breathing, hyperventilation, or rebreathing? Rebreathing 5. Explain why this type of breathing resulted in acidosis. Hypoventilation results in elevated CO 2 levels in the blood, H + levels increase and pH decreases. Metabolic Acidosis and Alkalosis Activity 7: Respiratory Response to Normal metabolism 1. What is the respiratory rate? 15 2. What is the blood pH? 7.4 3. Are the blood pH and P CO2 values within normal ranges? Yes Activity 8: Respiratory Response to Increased Metabolism 1. How did respiration change? BPM and tidal volume increased. 60: 17 70:19 80:21 2. How did blood pH change? 60:7.36 70:7.28 80:7.25 3. How did P CO2 change? 60:45 70:52 80:55 4. How did [H + ] change? 60:47 70:55 80:63 5. How did [HCO 3- ] change? 60:20 70:16 80:14.5 6. Explain why these changes took place as metabolic rate increased? More CO 2 results in the formation of more H+ lowering plasma pH, potentially causing acidosis. 7. Which metabolic rates caused pH levels to decrease to a condition of metabolic acidosis? 70 & 80 8. What were the pH values at each of these rates? 70:7.28 80:7.25 9. By the time the respiratory system fully compensated for acidosis, how would you expect the pH values to change? pH level will increase. Activity 9: Respiratory Response to Decreased Metabolism 1. How did respiration change? 40:13 30:11 20:9 2. How did blood pH change? 40:7.45 30:7.45 20:7.52 3. How did P CO2 change? 40:37 30:34 20:31 4. How did [H + ] change? 40:38 30:34 20:32 5. How did [HCO 3- ] change? 40:26 30:28 20:30 6. Explain why these changes took place as metabolic rate decreased? It results in less CO 2 being formed, making less H+ raisi Continue reading >>

[physioex Chapter 10 Exercise 4] Pex-10-04

[physioex Chapter 10 Exercise 4] Pex-10-04

Solved by ramonistry Exercise 10: Acid-Base Balance: Activity 4: Respiratory Responses to Metabolic Acidosis and Metabolic Alkalosis Lab Report Pre-lab Quiz Results You scored 100% by answering 4 out of 4 questions correctly. An increase in metabolic rate (without compensation) would result in You correctly answered: a. more carbon dioxide in the blood. Excessive vomiting results in You correctly answered: c. loss of acid, metabolic alkalosis. Which of the following is not acidic? You correctly answered: d. antacids Which of the following decreases the rate of metabolism? You correctly answered: b. lowered body temperature Experiment Results Predict Question: Predict Question 1: What do you think will happen when the metabolic rate is increased to 80 kcal/hr? Your answer : a. metabolic acidosis Predict Question 2: What do you think will happen when the metabolic rate is decreased to 20 kcal/hr? Your answer : d. Breaths per minute will decrease. Stop & Think Questions: The tidal volume and breaths per minute increased with increased metabolism because You correctly answered: b. there is more carbon dioxide being formed. Which body system is compensating for the metabolic alkalosis? You correctly answered: c. respiratory Experiment Data: Metabolic Rate (kcal/hr) BPM (breaths/min) Blood pH PCO2 [H+] in Blood [HCO3-] in Blood 50 15 7.41 40 40 24 60 17 7.34 45 47 20 80 21 7.26 55 63 14.50 40 13 7.45 37 38 26 20 9 7.49 31 32 30 Post-lab Quiz Results You scored 100% by answering 4 out of 4 questions correctly. What happened to the breathing when metabolism was increased? You correctly answered: d. The breaths per minute and the tidal volume increased. Which of the following is not a cause of metabolic acidosis? You correctly answered: b. constipation If PCO2 in the blood incre Continue reading >>

Acidosis/alkalosis

Acidosis/alkalosis

This article waslast modified on 31 January 2019. Acidosis and alkalosis are terms used to describe abnormal conditions when a patients blood pH may not fall within the healthy range. Measuring the hydrogen ion concentration, and calculating the pH , of blood is a way of finding out how acidic or alkaline the blood is. Normal blood pH must be within a narrow range of 7.35-7.45 so that the bodys metabolic processes can work properly and can deliver the right amount of oxygen to tissues. Many diseases and other conditions can cause a patients blood pH to fall outside of these healthy limits. In the human body, normal metabolism generates large quantities of acids (effectively compounds that produce a free hydrogen ion) that must be removed to keep a normal pH balance. Disruption of this balance can be caused by a build-up of acid or alkali (base) or by an increased loss of acid or alkali (see the diagram of taps and drains below). Alkalis, or bases, are compounds that remove a free hydrogen ion. Acidosis occurs when blood pH falls below 7.35, indicating an increase in hydrogen ion concentration. Alkalosis occurs when blood pH rises above 7.45, indicating a reduction in hydrogen ion concentration. Both of these conditions act as an alarm to the body; they trigger actions intended to restore the balance and to return the blood pH to its normal range. The major organs involved in regulating blood pH are the lungs and the kidneys. The lungs flush acid out of the body by exhaling carbon dioxide (CO2), which forms an acid when in solution (dissolved in the blood). Within physical limits, the body can raise and lower the rate of breathing to alter the amount of carbon dioxide that is breathed out. This can affect blood pH within seconds to minutes. The kidneys remove some acids Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Practice Essentials Metabolic acidosis is a clinical disturbance characterized by an increase in plasma acidity. Metabolic acidosis should be considered a sign of an underlying disease process. Identification of this underlying condition is essential to initiate appropriate therapy. (See Etiology, DDx, Workup, and Treatment.) Understanding the regulation of acid-base balance requires appreciation of the fundamental definitions and principles underlying this complex physiologic process. Go to Pediatric Metabolic Acidosis and Emergent Management of Metabolic Acidosis for complete information on those topics. Continue reading >>

Pathogenesis, Consequences, And Treatment Of Metabolic Acidosis In Chronic Kidney Disease

Pathogenesis, Consequences, And Treatment Of Metabolic Acidosis In Chronic Kidney Disease

The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2018 UpToDate, Inc. All topics are updated as new evidence becomes available and our peer review process is complete. INTRODUCTION — Most individuals produce approximately 15,000 mmol (considerably more with exercise) of carbon dioxide and 50 to 100 meq of nonvolatile acid each day. Acid-base balance is maintained by normal elimination of carbon dioxide by the lungs (which affects the partial pressure of carbon dioxide [PCO2]) and normal excretion of nonvolatile acid by the kidneys (which affects the plasma bicarbonate concentration). The hydrogen ion concentration of the blood is determined by the ratio of the PCO2 and plasma bicarbonate concentration. (See "Simple and mixed acid-base disorders", section on 'Introduction'.) Acidosis associated with chronic kidney disease (CKD) will be discussed in this topic. An overview of simple acid-base disorders and renal tubular acidosis, as well as the approach to patients with metabolic acidosis, are presented elsewhere. (See "Simple and mixed acid-base disorders" and "Overview and pathophysiology of renal tubular acidosis and the effect on potassium balance" and "Approach to the adult with metabolic acidosis" and "Approach to the child with metabolic acidosis".) ACID-BASE BALANCE IN CHRONIC KIDNEY DISEASE — Acid-base balance is normally maintained by the renal excretion of the daily acid load (about 1 meq/kg per day, derived mostly from the generation of sulfuric acid during the metabolism of sulf Continue reading >>

Metabolic Alkalosis In Patients With Renal Failure

Metabolic Alkalosis In Patients With Renal Failure

Introduction Alkalosis is most unusual in patients with advanced renal failure. When patients are also hyponatraemic, hypochloraemic and hypokalaemic, management can be a considerable challenge. The purpose of this report is to illustrate by means of three patients the potential for diagnostic uncertainty and therapeutic error in these metabolic settings and to outline some simple principles in diagnosis and management. Cases Patient 1 A 38-year-old man presented to the A&E department giving a history of vomiting and intermittent diarrhoea for 2 weeks. He could keep nothing down other than cider and water, and his urine output had fallen. His alcohol intake was excessive and he smoked heavily but he denied taking recreational drugs. His only medication was ranitidine. A known epileptic he had had a seizure 1 week previously. On several occasions in the past he had been admitted with drug overdoses. On examination his breath smelt of alcohol. He was restless but orientated with a Glasgow Coma Score (GCS) of 15/15. His blood pressure (BP) was 140/80 mmHg with a pulse of 90 beats/min in sinus rhythm. His jugular venous pressure (JVP) was visible 1 cm above the level of the manubrio–sternal joint. His respiratory and abdominal systems were unremarkable and neurological examination revealed only truncal ataxia. Blood results are shown in Table 1. In addition, his liver enzymes, amylase and thyroid hormones were within the normal range; calcium 2.33 mmol/l, phosphate 2.12 mmol/l, magnesium 0.77 mmol/l, creatine kinase 1111 U/l, random cortisol 1207 U/l, total cholesterol 3.4 mmol/l. Arterial blood revealed: pH 7.59, pO2 12.06 kPa (on air), pCO2 5.2 kPa, HCO3– 38.4 mmol/l and lactate 0.7 mmol/l. Serum was negative for opiates, benzodiazepines, cocaine, cannabinoids, salicy Continue reading >>

Respiratory Alkalosis

Respiratory Alkalosis

Respiratory alkalosis is a medical condition in which increased respiration elevates the blood pH beyond the normal range (7.35–7.45) with a concurrent reduction in arterial levels of carbon dioxide.[1][3] This condition is one of the four basic categories of disruption of acid–base homeostasis.[medical citation needed] Signs and symptoms[edit] Signs and symptoms of respiratory alkalosis are as follows:[4] Palpitation Tetany Convulsion Sweating Causes[edit] Respiratory alkalosis may be produced as a result of the following causes: Stress[1] Pulmonary disorder[2] Thermal insult[5] High altitude areas[6] Salicylate poisoning (aspirin overdose) [6] Fever[1] Hyperventilation (due to heart disorder or other, including improper mechanical ventilation)[1][7] Vocal cord paralysis (compensation for loss of vocal volume results in over-breathing/breathlessness).[8] Liver disease[6] Mechanism[edit] Carbonic-acid The mechanism of respiratory alkalosis generally occurs when some stimulus makes a person hyperventilate. The increased breathing produces increased alveolar respiration, expelling CO2 from the circulation. This alters the dynamic chemical equilibrium of carbon dioxide in the circulatory system. Circulating hydrogen ions and bicarbonate are shifted through the carbonic acid (H2CO3) intermediate to make more CO2 via the enzyme carbonic anhydrase according to the following reaction: This causes decreased circulating hydrogen ion concentration, and increased pH (alkalosis).[9][10] Diagnosis[edit] The diagnosis of respiratory alkalosis is done via test that measure the oxygen and carbon dioxide levels (in the blood), chest x-ray and a pulmonary function test of the individual.[1] The Davenport diagram allows clinicians or investigators to outline blood bicarbonate concentr Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. See also separate Lactic Acidosis and Arterial Blood Gases - Indications and Interpretations articles. Description Metabolic acidosis is defined as an arterial blood pH <7.35 with plasma bicarbonate <22 mmol/L. Respiratory compensation occurs normally immediately, unless there is respiratory pathology. Pure metabolic acidosis is a term used to describe when there is not another primary acid-base derangement - ie there is not a mixed acid-base disorder. Compensation may be partial (very early in time course, limited by other acid-base derangements, or the acidosis exceeds the maximum compensation possible) or full. The Winter formula can be helpful here - the formula allows calculation of the expected compensating pCO2: If the measured pCO2 is >expected pCO2 then additional respiratory acidosis may also be present. It is important to remember that metabolic acidosis is not a diagnosis; rather, it is a metabolic derangement that indicates underlying disease(s) as a cause. Determination of the underlying cause is the key to correcting the acidosis and administering appropriate therapy[1]. Epidemiology It is relatively common, particularly among acutely unwell/critical care patients. There are no reliable figures for its overall incidence or prevalence in the population at large. Causes of metabolic acidosis There are many causes. They can be classified according to their pathophysiological origin, as below. The table is not exhaustive but lists those that are most common or clinically important to detect. Increased acid Continue reading >>

Acid Base Statuses

Acid Base Statuses

A B Metabolic Acidosis (1) results from cold stress Respiratory Alkalosis (1) results from excessive CO2 blown off Body decr carbonic acid (1) results in slow respirations so that CO2 is retained Acidosis (1) symptoms (a) CNS depression (b) errors in judgment (c) disorientation (d) drowsiness (e) stupor (f) coma Hydrogen Ions excess (1) results in acidosis as pH falls below 7.35 (2) hydrogen ions are forced into the cells causing K+ to move into the cells Diabetic Ketoacidosis metabolic acidosis Metabolic Acidosis dehydration after an extended bout of diarrhea COPD respiratory acidosis Diarrhea (1) respirtory acidosis Anxiety (1)results in respiratory alkalosis (2) associated w/hyperventilation (2) during hyperventilation CO2 is blown off which lowers the amount of acid in the system Severe Asthma Respiratory Alkalosis Acute Renal Failure (1) metabolic acidosis (2) hypermagnesemia (3) hyperkalemia (4) hypocalcemia Diarrhea (1) metabolic acidosis (2) leads to meta acid because there is an over-elimination of bicarbonate Alkalosis (1) signs (a) tingling fingers, toes & face (b) estreme nervousness (c) twitching of muscles (d) tetany Severe Asthma respiratory acidosis Vomiting (1) metabolic alkalosis (2) leads to metabolic alkalosis as hydrochloric acid is lost from the stomach Aspirin metabolic acidosis Overdose of Morphine respiratory acisosis Vigorous Diuresis metabolic alkalosis End Stage Muscular Distrophy respiratory acidosis Severe Hypokalemia metabolic alkalosis Renal Failure (1) results in metabolic acisosis as fluid build up turns acidic Shock (1) metabolic acidosis (2) meta acid because acid is added to the system (3) anaerobic metabolic pathways result in lactate and hydrogen irons (forming lactic acid) Hyperventilation (1) respiratory alkalosis (2) leads to re Continue reading >>

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