Feeder pathways to glycolysis US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Feeder pathways to glycolysis. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Feeder pathways to glycolysis US Medical PG Question 1: A 20-year-old male with no significant medical history comes to you with a urine positive for fructose. He does not have diabetes mellitus. Which enzyme is most likely to be deficient in this patient?
- A. Pyruvate kinase
- B. Lactase
- C. Fructokinase (Correct Answer)
- D. Aldolase B
Feeder pathways to glycolysis Explanation: ***Fructokinase***
- A urine positive for **fructose** without symptoms of diabetes mellitus (i.e., **benign fructosuria**) is characteristic of a **fructokinase deficiency**.
- **Fructokinase** is the enzyme responsible for the first step in fructose metabolism, converting **fructose to fructose-1-phosphate**.
*Pyruvate kinase*
- Deficiency of **pyruvate kinase** primarily affects **glycolysis** in red blood cells and leads to **hemolytic anemia**, not fructosuria.
- This enzyme converts **phosphoenolpyruvate to pyruvate**.
*Lactase*
- **Lactase** is an enzyme that digests **lactose** (milk sugar) into glucose and galactose.
- A deficiency in lactase causes **lactose intolerance**, presenting with gastrointestinal symptoms like bloating and diarrhea after consuming dairy products, not fructose in the urine.
*Aldolase B*
- A deficiency in **aldolase B** leads to **hereditary fructose intolerance**, a severe condition where **fructose-1-phosphate accumulates** after fructose ingestion.
- This typically presents with symptoms such as **hypoglycemia**, vomiting, jaundice, and liver damage, which are not described in this benign case of fructosuria.
Feeder pathways to glycolysis US Medical PG Question 2: A 6-month-old boy is brought to the emergency department by his mother because of recurrent vomiting and yellowing of his eyes. The mother says that he has been eating poorly since she started weaning him off of breast milk 5 days ago. At this time, mashed vegetables and fruits were added to his diet. Examination shows scleral jaundice and dry mucous membranes. The tip of the liver is palpable 4 cm below the right costal margin. His serum glucose concentration is 47 mg/dL, serum alanine aminotransferase is 55 U/L, and serum aspartate aminotransferase is 66 U/L. Which of the following enzymes is most likely deficient?
- A. Fructokinase
- B. Glucose-6-phosphatase
- C. Galactokinase
- D. Galactose-1 phosphate uridyltransferase
- E. Aldolase B (Correct Answer)
Feeder pathways to glycolysis Explanation: ***Aldolase B***
- The symptoms, including **jaundice**, vomiting, **hepatomegaly**, and **hypoglycemia** following the introduction of solid foods (specifically fruits and vegetables containing **fructose**), are classic for **hereditary fructose intolerance**.
- **Aldolase B** is crucial for metabolizing fructose in the liver; its deficiency leads to the buildup of **fructose-1-phosphate**, which is toxic to hepatocytes and inhibits glucose production.
*Fructokinase*
- Fructokinase deficiency causes **essential fructosuria**, a benign condition characterized by fructose in the urine, but without the severe metabolic disturbances like hypoglycemia and liver damage seen in this patient.
- This condition does not typically present with the **jaundice**, vomiting, and liver enlargement found in the given case.
*Glucose-6-phosphatase*
- A deficiency in **glucose-6-phosphatase** causes **Type I glycogen storage disease (Von Gierke disease)**, which presents with severe hypoglycemia and hepatomegaly.
- However, it does not typically cause the **jaundice** or acute symptoms triggered by the introduction of solid foods containing fructose as described in this case.
*Galactokinase*
- Deficiency of galactokinase leads to **Type II galactosemia**, characterized primarily by **cataracts** and galactosemia, but typically without the profound liver damage, jaundice, or acute hypoglycemia seen here.
- The symptoms in this case are related to **fructose** intake, not galactose.
*Galactose-1 phosphate uridyltransferase*
- Deficiency in **galactose-1-phosphate uridyltransferase** causes **classic galactosemia**, which presents with **jaundice**, hepatosplenomegaly, vomiting, and cataracts, often triggered by lactose (galactose) intake.
- While it shares some symptoms with the patient's presentation, the trigger of symptoms upon introducing fruits and vegetables (high in fructose) points specifically to an issue with **fructose metabolism**, not galactose.
Feeder pathways to glycolysis US Medical PG Question 3: A 59-year-old man comes to the physician because of bilateral blurry vision and difficulty driving at night that has been worsening progressively over the past 5 months. He has hypertension, type 2 diabetes mellitus, and hyperlipidemia. His hemoglobin A1c concentration is 8.9 mg/dL. A slit-lamp shows cloudy opacities of the lenses bilaterally. The patient's eye condition is most likely due to increased activity of which of the following enzymes?
- A. Galactokinase
- B. Aldolase B
- C. Sorbitol dehydrogenase
- D. Aldose reductase (Correct Answer)
- E. Glucokinase
Feeder pathways to glycolysis Explanation: **Aldose reductase**
- The patient's presentation of **bilateral blurry vision**, **difficulty driving at night**, and **cloudy lens opacities** in the context of poorly controlled diabetes (HbA1c 8.9%) is classic for **diabetic cataracts**.
- **Aldose reductase** is the key enzyme in the polyol pathway that converts **glucose to sorbitol**. In hyperglycemia, increased activity of this enzyme leads to **sorbitol accumulation** in lens cells, causing osmotic damage and cataract formation.
*Galactokinase*
- **Galactokinase** is involved in galactose metabolism, converting galactose to galactose-1-phosphate.
- Deficiencies in this enzyme can lead to **galactosemia** and early-onset cataracts, but this typically presents in infancy or early childhood, not in a 59-year-old with diabetes.
*Aldolase B*
- **Aldolase B** is an enzyme critical for the metabolism of fructose in the liver.
- Its deficiency causes **hereditary fructose intolerance**, leading to symptoms like hypoglycemia, jaundice, and vomiting upon fructose ingestion, which are not relevant to this patient's eye condition.
*Sorbitol dehydrogenase*
- **Sorbitol dehydrogenase** converts **sorbitol to fructose** in the polyol pathway.
- While part of the same pathway, its activity prevents sorbitol accumulation, so an *increase* in its activity would likely be protective against diabetic complications, not causative of cataracts.
*Glucokinase*
- **Glucokinase** (also known as hexokinase IV) is an enzyme that phosphorylates glucose to glucose-6-phosphate, mainly in the liver and pancreatic beta cells.
- Mutations in glucokinase can cause various forms of diabetes, but its activity is primarily involved in glucose sensing and metabolism, not directly in the pathogenesis of diabetic cataracts through increased polyol pathway flux.
Feeder pathways to glycolysis US Medical PG Question 4: A 65-year-old male prisoner goes on a hunger strike to protest the conditions of his detainment. After 5 days without food, he suffers a seizure for which he is taken into a medical facility. On physical examination, he looks pale and diaphoretic. His blood glucose level is 50 mg/dL. In order to keep a constant supply of energy to his brain, which of the following molecules is his liver releasing into the bloodstream?
- A. Glycogen
- B. Glucose-6-phosphate
- C. ß-hydroxybutyric acid (Correct Answer)
- D. Fatty acids
- E. Glucose-1-phosphate
Feeder pathways to glycolysis Explanation: ***ß-hydroxybutyric acid***
- After 5 days of a hunger strike, **glycogen stores** are depleted, forcing the body to rely on **fatty acid oxidation** and **ketone body production** in the liver as an alternative fuel source for the brain.
- **ß-hydroxybutyrate** is one of the primary ketone bodies released by the liver into the bloodstream to provide energy, especially for the brain, during prolonged fasting.
*Glycogen*
- **Glycogenolysis** (breakdown of glycogen) is a short-term response to low blood glucose and supplies glucose for only about 24-36 hours of fasting. After 5 days, **hepatic glycogen stores** would be largely depleted.
- The liver releases **free glucose** into the bloodstream, not intact glycogen, from glycogen breakdown.
*Glucose-6-phosphate*
- **Glucose-6-phosphate** is an intermediate in glycolysis and gluconeogenesis, but it is not directly released into the bloodstream by the liver.
- It must be converted to **free glucose** by glucose-6-phosphatase before it can exit the hepatocyte and enter circulation.
*Fatty acids*
- The liver takes up **fatty acids** from adipose tissue breakdown during prolonged fasting to convert them into **ketone bodies**.
- While fatty acids are a major energy source for other tissues, the **brain cannot directly utilize fatty acids** for energy due to the inability of long-chain fatty acids to cross the blood-brain barrier.
*Glucose-1-phosphate*
- **Glucose-1-phosphate** is an intermediate formed during the breakdown of glycogen (glycogenolysis).
- Like glucose-6-phosphate, it is not directly released into the bloodstream but is further metabolized within the hepatocyte, eventually leading to the release of **free glucose**.
Feeder pathways to glycolysis US Medical PG Question 5: A newborn undergoing the standard screening tests is found to have a positive test for reducing sugars. Further testing is performed and reveals that the patient does not have galactosemia, but rather is given a diagnosis of fructosuria. What levels of enzymatic activity are altered in this patient?
- A. Hexokinase decreased; fructokinase decreased
- B. Hexokinase unchanged; fructokinase unchanged
- C. Hexokinase increased; fructokinase increased
- D. Hexokinase increased; fructokinase decreased
- E. Hexokinase unchanged; fructokinase decreased (Correct Answer)
Feeder pathways to glycolysis Explanation: ***Hexokinase unchanged; fructokinase decreased***
- **Essential fructosuria** is caused by a deficiency in **fructokinase**, the enzyme responsible for the first step of fructose metabolism (fructose → fructose-1-phosphate).
- This results in **decreased or absent fructokinase activity**, leading to fructose accumulation in blood and urine (positive reducing sugar test).
- **Hexokinase activity remains unchanged** - there is no upregulation or compensatory increase in hexokinase. The enzyme maintains its normal baseline activity.
- Essential fructosuria is a **benign, asymptomatic condition** with no metabolic stress, so no compensatory enzyme changes occur.
- The small amount of fructose that needs metabolism can be handled by normal baseline hexokinase activity (hexokinase has broad substrate specificity).
*Hexokinase decreased; fructokinase decreased*
- While **fructokinase is decreased** in essential fructosuria, hexokinase activity is not decreased.
- Hexokinase is a constitutively expressed glycolytic enzyme whose activity does not change in this benign condition.
*Hexokinase unchanged; fructokinase unchanged*
- This is incorrect because **fructokinase activity is specifically decreased** in essential fructosuria, which is the defining enzymatic defect of the condition.
- The decreased fructokinase activity causes fructose to accumulate and appear in the urine.
*Hexokinase increased; fructokinase increased*
- **Fructokinase is decreased, not increased** - an increase would prevent the fructose accumulation characteristic of this condition.
- Hexokinase activity does not increase as essential fructosuria causes no metabolic stress requiring compensation.
*Hexokinase increased; fructokinase decreased*
- While **fructokinase is decreased** in essential fructosuria, hexokinase activity does not increase.
- This is a benign condition with no compensatory enzyme upregulation - hexokinase maintains normal baseline activity levels.
Feeder pathways to glycolysis US Medical PG Question 6: An 11-year-old boy is brought to the emergency room with acute abdominal pain and hematuria. Past medical history is significant for malaria. On physical examination, he has jaundice and a generalized pallor. His hemoglobin is 5 g/dL, and his peripheral blood smear reveals fragmented RBC, microspherocytes, and eccentrocytes (bite cells). Which of the following reactions catalyzed by the enzyme is most likely deficient in this patient?
- A. Glucose-1-phosphate + UTP → UDP-glucose + pyrophosphate
- B. Glucose + ATP → Glucose-6-phosphate + ADP + H+
- C. D-glucose 6-phosphate → D-fructose-6-phosphate
- D. Glucose-6-phosphate + H2O → glucose + Pi
- E. D-glucose-6-phosphate + NADP+ → 6-phospho-D-glucono-1,5-lactone + NADPH + H+ (Correct Answer)
Feeder pathways to glycolysis Explanation: ***D-glucose-6-phosphate + NADP+ → 6-phospho-D-glucono-1,5-lactone + NADPH + H+***
- This reaction is catalyzed by **glucose-6-phosphate dehydrogenase (G6PD)**, an enzyme critical for the production of **NADPH** in the **pentose phosphate pathway**.
- **NADPH** is essential for reducing **oxidative stress** in red blood cells. A deficiency in G6PD leads to increased susceptibility to hemolysis, especially under oxidative triggers like malaria, resulting in symptoms such as **acute hemolytic anemia**, jaundice, and specific morphological changes (e.g., **fragmented RBCs**, **microspherocytes**, and **eccentrocytes**, also known as **bite cells**).
*Glucose-1-phosphate + UTP → UDP-glucose + pyrophosphate*
- This reaction is catalyzed by **UDP-glucose pyrophosphorylase** and is important for **glycogen synthesis**.
- A deficiency in this enzyme would primarily affect glycogen metabolism and would not explain the **hemolytic anemia** or the characteristic red blood cell morphology seen in the patient.
*Glucose + ATP → Glucose-6-phosphate + ADP + H+*
- This reaction is catalyzed by **hexokinase**, the first committed step in **glycolysis**.
- While hexokinase deficiency can cause **hemolytic anemia**, it generally presents with chronic, moderate anemia and does not typically involve the specific red blood cell morphology (eccentrocytes/bite cells) associated with oxidative damage found in G6PD deficiency.
*D-glucose 6-phosphate → D-fructose-6-phosphate*
- This reaction is catalyzed by **phosphoglucose isomerase** (also known as phosphohexose isomerase) and is part of **glycolysis**.
- A deficiency in this enzyme would impair glycolysis and lead to **hemolytic anemia**, but its clinical presentation and RBC morphology differ from what is typically seen in G6PD deficiency, particularly the absence of oxidative stress markers like bite cells.
*Glucose-6-phosphate + H2O → glucose + Pi*
- This reaction is catalyzed by **glucose-6-phosphatase**, an enzyme found primarily in the liver and kidney, responsible for the final step in **gluconeogenesis** and glycogenolysis to release free glucose into the bloodstream.
- A deficiency in glucose-6-phosphatase leads to **glycogen storage disease type I (Von Gierke's disease)**, characterized by **hypoglycemia**, **lactic acidosis**, and hepatomegaly, not hemolytic anemia.
Feeder pathways to glycolysis US Medical PG Question 7: A 3-week-old newborn is brought to the pediatrician by his mother. His mother is concerned about her son’s irritability and vomiting, particularly after breastfeeding him. The infant was born at 39 weeks via spontaneous vaginal delivery. His initial physical was benign. Today the newborn appears mildly jaundiced with palpable hepatomegaly, and his eyes appear cloudy, consistent with the development of cataracts. The newborn is also in the lower weight-age percentile. The physician considers a hereditary enzyme deficiency and orders blood work and a urinalysis to confirm his diagnosis. He recommends that milk and foods high in galactose and/or lactose be eliminated from the diet. Which of the following is the most likely deficient enzyme in this metabolic disorder?
- A. Aldose reductase
- B. Galactose-1-phosphate uridyl transferase (Correct Answer)
- C. UDP-galactose-4-epimerase
- D. Galactokinase
- E. Glucose-6-phosphate dehydrogenase
Feeder pathways to glycolysis Explanation: ***Galactose-1-phosphate uridyl transferase***
- The constellation of symptoms including **vomiting**, **irritability**, **jaundice**, **hepatomegaly**, **cataracts**, and **failure to thrive** in a neonate, with improvement upon eliminating galactose/lactose from the diet, is highly characteristic of **classic galactosemia**.
- **Classic galactosemia** is caused by a deficiency in **galactose-1-phosphate uridyl transferase (GALT)**, leading to the accumulation of galactose-1-phosphate, which is toxic to various tissues.
*Aldose reductase*
- This enzyme converts galactose to **galactitol**, which can accumulate in the lens and cause **cataracts** in all forms of galactosemia if left untreated.
- However, isolated aldose reductase deficiency does not explain the full spectrum of severe systemic symptoms like hepatomegaly, jaundice, and failure to thrive observed in this neonate, which are indicative of classic galactosemia.
*UDP-galactose-4-epimerase*
- Deficiency in **UDP-galactose-4-epimerase (GALE)**, also known as epimerase deficiency galactosemia, has a wide range of severity.
- While it can present with similar symptoms to GALT deficiency, its severe form is rarer, and the classic, pronounced presentation described here is more commonly associated with GALT deficiency.
*Galactokinase*
- Deficiency in **galactokinase (GALK)** causes **Type II galactosemia**, which primarily manifests as **cataracts** due to galactitol accumulation.
- It typically does not present with the severe hepatic (jaundice, hepatomegaly) or systemic symptoms (vomiting, failure to thrive) seen in classic galactosemia.
*Glucose-6-phosphate dehydrogenase*
- **Glucose-6-phosphate dehydrogenase (G6PD) deficiency** primarily causes **hemolytic anemia** triggered by certain drugs, infections, or fava beans.
- It does not present with the specific constellation of symptoms related to galactose metabolism, such as cataracts, hepatomegaly, and vomiting upon milk ingestion, as described in this case.
Feeder pathways to glycolysis US Medical PG Question 8: A 7-day-old female newborn is brought to the physician because of lethargy, vomiting, poor feeding, and diarrhea for 4 days. She was born at 39 weeks' gestation. Vital signs are within normal limits. Bilateral cataracts and icterus are present. Examination shows jaundice of the skin, and the liver is palpated 5-cm below the right costal margin. Muscle tone is decreased in all extremities. Serum glucose concentration is 40 mg/dL. Which of the following metabolites is most likely to be increased in this patient?
- A. Branched-chain amino acids
- B. Limit dextrins
- C. Galactose-1-phosphate (Correct Answer)
- D. Sphingomyelin
- E. Uric acid
Feeder pathways to glycolysis Explanation: ***Galactose-1-phosphate***
- The constellation of **neonatal lethargy, vomiting, poor feeding, diarrhea, jaundice, hepatomegaly, cataracts, decreased muscle tone**, and **hypoglycemia** in a 7-day-old newborn strongly points to **classic galactosemia**.
- In classic galactosemia, there is a deficiency of **galactose-1-phosphate uridyltransferase (GALT)**, leading to the accumulation of **galactose-1-phosphate** as well as galactitol and galactose.
*Branched-chain amino acids*
- Elevated **branched-chain amino acids** (leucine, isoleucine, valine) are characteristic of **maple syrup urine disease**.
- While maple syrup urine disease can present with lethargy, poor feeding, and neurologic symptoms, it does not typically cause **cataracts, jaundice**, or **hepatomegaly**.
*Limit dextrins*
- **Limit dextrins** are intermediate products of starch digestion and accumulated in glycogen storage diseases, particularly **Cori disease (Type III glycogen storage disease)** or **Anderson disease (Type IV glycogen storage disease)**.
- While glycogen storage diseases can cause **hypoglycemia** and **hepatomegaly**, they do not typically present with **cataracts, vomiting, diarrhea**, or prominent early onset jaundice like galactosemia.
*Sphingomyelin*
- Accumulation of **sphingomyelin** is characteristic of **Niemann-Pick disease**, a lysosomal storage disorder.
- While Niemann-Pick disease can present with hepatosplenomegaly and neurologic regression, it typically does not cause acute neonatal distress with **cataracts, acute jaundice**, or **vomiting and diarrhea** as seen here.
*Uric acid*
- Elevated **uric acid** is a hallmark of disorders such as **Lesch-Nyhan syndrome** or conditions causing increased purine breakdown or decreased excretion.
- Lesch-Nyhan syndrome presents with self-mutilation, hypotonia, and cognitive deficits, which do not align with the described symptoms. Hyperuricemia is not a feature of galactosemia.
Feeder pathways to glycolysis US Medical PG Question 9: A 12-year-old boy and his siblings are referred to a geneticist for evaluation of a mild but chronic hemolytic anemia that has presented with fatigue, splenomegaly, and scleral icterus. Coombs test is negative and blood smear does not show any abnormal findings. An enzymatic panel is assayed, and pyruvate kinase is found to be mutated on both alleles. The geneticist explains that pyruvate kinase functions in glycolysis and is involved in a classic example of feed-forward regulation. Which of the following metabolites is able to activate pyruvate kinase?
- A. Fructose-1,6-bisphosphate (Correct Answer)
- B. Alanine
- C. ATP
- D. Glucose-6-phosphate
- E. Glyceraldehyde-3-phosphate
Feeder pathways to glycolysis Explanation: ***Fructose-1,6-bisphosphate***
- **Fructose-1,6-bisphosphate** is a potent **allosteric activator** of pyruvate kinase. This is an example of **feed-forward activation**, where a product of an early irreversible step in glycolysis (catalyzed by phosphofructokinase-1) activates a later enzyme (pyruvate kinase) in the pathway.
- This activation ensures that substrates for the later steps of glycolysis are rapidly utilized when earlier steps are highly active, matching the rate of metabolite flow and increasing the overall efficiency of glycolysis for energy production.
*Alanine*
- **Alanine** is an **inhibitor** of pyruvate kinase, not an activator. It serves as an indicator of a high cellular energy state and ample amino acid supply.
- High levels of alanine signal the cell that there is sufficient energy and building blocks, thus **shutting down** glycolysis at the pyruvate kinase step to conserve glucose for other needs like glycogen synthesis.
*ATP*
- **ATP** (adenosine triphosphate) is an **allosteric inhibitor** of pyruvate kinase. High ATP levels signal a high energy state in the cell.
- When the cell has sufficient energy, ATP binds to a regulatory site on pyruvate kinase, reducing its activity and **slowing down glycolysis** to prevent overproduction of ATP.
*Glucose-6-phosphate*
- **Glucose-6-phosphate** is an intermediate in glycolysis but does not directly activate pyruvate kinase. It can act as an allosteric inhibitor of hexokinase, the first enzyme in glycolysis, but not pyruvate kinase.
- Its accumulation typically signifies a **backup** in the glycolytic pathway (e.g., due to downstream inhibition), leading to a *reduction* in overall glucose flux rather than a direct activation of pyruvate kinase.
*Glyceraldehyde-3-phosphate*
- **Glyceraldehyde-3-phosphate** is an intermediate in glycolysis, but it does not directly activate pyruvate kinase. It is a substrate for glyceraldehyde-3-phosphate dehydrogenase.
- While its presence indicates active glycolysis, it does not exert a specific allosteric regulatory effect on pyruvate kinase in the way fructose-1,6-bisphosphate does.
Feeder pathways to glycolysis US Medical PG Question 10: To maintain blood glucose levels even after glycogen stores have been depleted, the body, mainly the liver, is able to synthesize glucose in a process called gluconeogenesis. Which of the following reactions of gluconeogenesis requires an enzyme different from glycolysis?
- A. Fructose 1,6-bisphosphate --> Fructose-6-phosphate (Correct Answer)
- B. Glyceraldehyde 3-phosphate --> 1,3-bisphosphoglycerate
- C. 2-phosphoglycerate --> 3-phosphoglycerate
- D. Dihydroxyacetone phosphate --> Glyceraldehyde 3-phosphate
- E. Phosphoenolpyruvate --> 2-phosphoglycerate
Feeder pathways to glycolysis Explanation: ***Fructose 1,6-bisphosphate --> Fructose-6-phosphate***
- This reaction in gluconeogenesis is catalyzed by **fructose 1,6-bisphosphatase**, which is distinct from **phosphofructokinase-1** that catalyzes the reverse reaction in glycolysis.
- This step is one of the three **irreversible steps** in glycolysis that must be bypassed by different enzymes in gluconeogenesis to ensure the unidirectional flow of the pathway.
*Glyceraldehyde 3-phosphate --> 1,3-bisphosphoglycerate*
- This reaction is catalyzed by **Glyceraldehyde 3-phosphate dehydrogenase** in both glycolysis and gluconeogenesis, as it is a **reversible step**.
- In gluconeogenesis, the equilibrium is shifted towards the formation of glyceraldehyde 3-phosphate due to the low concentration of products.
*2-phosphoglycerate --> 3-phosphoglycerate*
- This is a reversible isomerization reaction catalyzed by **phosphoglycerate mutase** in both glycolysis and gluconeogenesis.
- No unique enzyme is required for gluconeogenesis at this step.
*Dihydroxyacetone phosphate --> Glyceraldehyde 3-phosphate*
- This reversible interconversion between these two triose phosphates is catalyzed by **triose phosphate isomerase** in both pathways.
- These molecules are in equilibrium and can be readily converted from one to the other.
*Phosphoenolpyruvate --> 2-phosphoglycerate*
- This is a reversible reaction catalyzed by **enolase** in both glycolysis and gluconeogenesis.
- No distinct enzyme is needed for this step in gluconeogenesis.
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