Molecular Pathology — MCQs

Molecular Pathology Indian Medical PG Practice Questions and MCQs

Question 31: A 22-year-old woman presents with congenital anemia requiring multiple RBC transfusions for many years. On physical examination, her skin has a bronze color and liver function tests show reduced serum albumin. Which of the following findings would most likely appear in a liver biopsy specimen?

A. Amyloid in portal triads
B. Bilirubin in canaliculi
C. Glycogen in hepatocytes
D. Hemosiderin in hepatocytes (Correct Answer)

Explanation: The clinical presentation of a young patient with chronic anemia requiring multiple blood transfusions, bronze skin pigmentation, and liver dysfunction (hypoalbuminemia) is a classic description of **Secondary Hemochromatosis (Hemosiderosis)**. **1. Why the Correct Answer is Right:** Each unit of transfused blood contains approximately 200–250 mg of iron. Since the human body lacks an active mechanism to excrete excess iron, chronic transfusion therapy leads to systemic iron overload [4]. The excess iron is stored in the form of **hemosiderin** (an iron-storage complex) within the mononuclear phagocytic system and parenchymal cells [2]. In the liver, hemosiderin initially accumulates in Kupffer cells and eventually in **hepatocytes**, leading to oxidative stress, fibrosis, and cirrhosis [1]. On biopsy, this is visualized as golden-brown granules, which stain positive (blue) with **Prussian Blue** [1]. **2. Why Incorrect Options are Wrong:** * **A. Amyloid:** Amyloidosis is associated with chronic inflammatory conditions (AA) or plasma cell dyscrasias (AL), not chronic transfusion. * **B. Bilirubin:** Canalicular bilirubin stasis (cholestasis) occurs in obstructive jaundice or certain drug-induced liver injuries, not typically in iron overload. * **C. Glycogen:** Glycogen accumulation is seen in Glycogen Storage Diseases (GSDs) or poorly controlled diabetes (Mauriac syndrome), presenting with hepatomegaly but not bronze skin. **3. NEET-PG High-Yield Pearls:** * **Classic Triad of Hemochromatosis:** Bronze skin, Cirrhosis, and Diabetes Mellitus ("Bronze Diabetes") [3]. * **Stain of Choice:** Prussian Blue (Perls' stain) identifies ferric iron [1]. * **Primary vs. Secondary:** Primary (Hereditary) Hemochromatosis is most commonly due to a mutation in the **HFE gene (C282Y)** on Chromosome 6 [3]. * **Cardiac Involvement:** Iron overload is a major cause of restrictive cardiomyopathy in these patients. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 854-855. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 394-395. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, p. 858. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 648.

Question 32: Mutation in the gene encoding Dystrophin is known to cause all the following except?

A. Duchenne muscular dystrophy
B. Becker muscular dystrophy
C. Dilated cardiomyopathy
D. Hypertrophic cardiomyopathy (Correct Answer)

Explanation: **Explanation:** The **Dystrophin gene** (located on the short arm of the X chromosome, **Xp21**) is the largest known human gene. It encodes dystrophin, a vital structural protein that links the cytoskeleton of a muscle fiber to the surrounding extracellular matrix through the cell membrane. **Why Option D is correct:** **Hypertrophic Cardiomyopathy (HCM)** is primarily a disease of the **sarcomere**. It is most commonly caused by mutations in genes encoding proteins of the contractile apparatus, such as **Beta-myosin heavy chain (MYH7)** and **Myosin-binding protein C (MYBPC3)**. It is not associated with dystrophin mutations. **Why the other options are incorrect:** * **A & B (DMD and BMD):** These are the classic "dystrophinopathies." **Duchenne Muscular Dystrophy (DMD)** results from **frameshift mutations** leading to a total absence of dystrophin (severe phenotype) [1]. **Becker Muscular Dystrophy (BMD)** results from **non-frameshift mutations**, leading to a truncated but partially functional protein (milder phenotype) [1]. * **C (Dilated Cardiomyopathy):** Dystrophin is essential for the mechanical stability of both skeletal and cardiac myocytes. Mutations can lead to **X-linked Dilated Cardiomyopathy (DCM)**, often occurring even in the absence of overt skeletal muscle weakness, as the weakened cardiac sarcolemma leads to progressive myocyte death and fibrosis. **NEET-PG High-Yield Pearls:** * **Inheritance:** X-linked Recessive. * **DMD Diagnosis:** Elevated Serum Creatine Kinase (CK) levels (present from birth); Muscle biopsy shows variation in fiber size and replacement by fat/fibrosis (**Pseudohypertrophy**). * **Gower’s Sign:** Classic clinical finding in DMD due to proximal muscle weakness. * **Death in DMD:** Usually occurs due to respiratory failure or heart failure (DCM). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1244-1245.

Question 33: Given below is the histopathology of liver biopsy of hemochromatosis. Which of the following stain is used to detect iron deposition?

A. Alcian blue stain
B. Prussian blue stain (Correct Answer)
C. Crystal violet stain
D. Von Kossa stain

Explanation: ***Prussian blue stain*** - **Prussian blue (Perls') stain** is the gold standard for detecting **iron/hemosiderin** in tissue sections and is essential for diagnosing hemochromatosis. - The stain works by reacting **ferric iron** with **potassium ferrocyanide** to form a characteristic **blue precipitate** that highlights iron deposits. *Alcian blue stain* - This stain is used to detect **acid mucopolysaccharides** and **mucins**, not iron deposits. - It produces a **blue color** for mucoid substances but does not react with **hemosiderin** or iron. *Crystal violet stain* - Primarily used to demonstrate **amyloid deposits** through **metachromasia** (color change from purple to pink). - Has no affinity for **iron** or **hemosiderin** and would not be useful in hemochromatosis diagnosis. *Von Kossa stain* - This stain is specifically used to detect **calcium deposits** in tissues, not iron. - It works by demonstrating **phosphates** and **carbonates** associated with calcium, producing a **black precipitate**.

Question 34: Councilman bodies are formed due to which process?

A. Necrosis
B. Cirrhosis
C. Apoptosis (Correct Answer)
D. Necroptosis

Explanation: **Explanation:** **Correct Answer: C. Apoptosis** **Councilman bodies** (also known as acidophilic bodies or apoptotic bodies) are the hallmark histological feature of individual hepatocyte death via **apoptosis** [1]. When a hepatocyte undergoes apoptosis, it shrinks, its nucleus undergoes pyknosis and karyorrhexis, and the cytoplasm becomes intensely eosinophilic (pink-staining) due to organelle condensation [1], [2]. These shrunken, pyknotic cells are then extruded into the hepatic sinusoids. They are most classically associated with **Yellow Fever**, but are also frequently seen in **Viral Hepatitis** (especially Acute Hepatitis) [1]. **Why other options are incorrect:** * **Necrosis:** Unlike apoptosis, necrosis involves cell swelling (oncosis), membrane rupture, and significant inflammation [2]. While "bridging necrosis" or "piecemeal necrosis" occurs in hepatitis, Councilman bodies specifically represent the programmed cell death pathway [1]. * **Cirrhosis:** This is a chronic, end-stage pathological state characterized by diffuse fibrosis and regenerative nodules. While apoptosis may occur during the progression of liver disease, cirrhosis describes the structural architectural change, not the cellular process of forming acidophilic bodies. * **Necroptosis:** This is a hybrid of necrosis and apoptosis (programmed necrosis). While it plays a role in some inflammatory diseases, it is not the mechanism responsible for the formation of classical Councilman bodies. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Councilman bodies appear as small, round, intensely eosinophilic bodies lacking a nucleus or containing nuclear fragments [1]. * **Key Association:** Yellow Fever (Classic association) and Viral Hepatitis [1]. * **Staining:** They stain bright red with H&E stain. * **Mechanism:** Mediated by Caspases (the executioners of apoptosis) [2]. * **Related Finding:** **Mallory-Denk bodies** (found in Alcoholic Hepatitis) are composed of damaged intermediate filaments (cytokeratin), whereas Councilman bodies are apoptotic cells. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 386-387. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 63-69.

Question 35: Liquefactive necrosis is seen in which of the following organs?

A. Kidney
B. Heart
C. Cerebrum (Correct Answer)
D. Intestine

Explanation: **Explanation:** **Liquefactive necrosis** is characterized by the transformation of the tissue into a liquid, viscous mass. This occurs due to the digestion of dead cells by hydrolytic enzymes. **Why Cerebrum is Correct:** In the **Central Nervous System (CNS)**, hypoxic cell death (infarction) uniquely results in liquefactive necrosis [1]. This is attributed to two main factors: 1. **High Lipid Content:** The brain is rich in lipids and low in supportive connective tissue. 2. **Enzymatic Digestion:** Microglial cells (the brain's macrophages) release powerful lysosomal enzymes that rapidly digest the necrotic tissue, leaving a fluid-filled cavity [1]. **Why Other Options are Incorrect:** * **Kidney & Heart:** These solid organs typically undergo **Coagulative Necrosis** following an infarct. In this process, the basic structural outline of the tissue is preserved for several days because the injury denatures both structural proteins and enzymes, blocking proteolysis. * **Intestine:** Ischemic injury to the bowel usually leads to **Gangrenous Necrosis**. While this starts as coagulative necrosis, if a bacterial infection superimposes, it can progress to "wet gangrene" (which has a liquefactive component). However, the primary classic example for liquefactive necrosis in exams remains the brain. **High-Yield NEET-PG Pearls:** * **Exceptions:** Liquefactive necrosis is seen in two primary scenarios: **CNS Infarcts** and **Abscesses** (due to neutrophilic enzymes in pyogenic infections). * **Coagulative Necrosis** is the most common pattern of necrosis in all organs *except* the brain. * **Morphology:** The end result of liquefactive necrosis in the brain is the formation of a **cystic space** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1268-1269.

Question 36: Which is the most common chromosomal anomaly seen?

A. Down's syndrome (Correct Answer)
B. Turner's syndrome
C. Klinefelter's syndrome
D. Edward's syndrome

Explanation: **Explanation:** **1. Why Down’s Syndrome is Correct:** Down’s syndrome (Trisomy 21) is the most common chromosomal disorder and the leading genetic cause of intellectual disability [1]. It occurs in approximately **1 in 700 to 1 in 800 live births** [2]. The high prevalence is attributed to the fact that Trisomy 21 is more compatible with postnatal survival compared to other autosomal trisomies [4]. The most common mechanism is **meiotic non-disjunction** (95% of cases), strongly associated with advanced maternal age [1]. **2. Why Other Options are Incorrect:** * **Turner’s Syndrome (45,X):** This is the most common sex chromosome abnormality in females, but its incidence is lower (approx. 1 in 2,500 live births) [1]. Notably, 99% of 45,X conceptuses result in spontaneous abortion. * **Klinefelter’s Syndrome (47,XXY):** This is the most common cause of hypogonadism in males, occurring in about 1 in 1,000 live births [3]. While common, it is statistically less frequent than Down’s syndrome. * **Edward’s Syndrome (Trisomy 18):** This is the second most common autosomal trisomy, but it is much rarer (1 in 6,000 to 8,000 live births) and carries a very poor prognosis, with most infants not surviving past the first year [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of Down’s:** Maternal meiotic non-disjunction (occurs during Meiosis I). * **Robertsonian Translocation:** Accounts for 4% of cases; involves chromosomes 14 and 21 [2]. * **Screening Markers:** In the first trimester, look for **increased Nuchal Translucency** and **decreased PAPP-A**. In the second trimester (Quadruple screen), **AFP and Estriol are decreased**, while **hCG and Inhibin-A are increased**. * **Associated Risks:** Early-onset Alzheimer’s (APP gene on Ch 21), Acute Leukemia (AMKL/M7 in children <3 years; ALL in older children), and Endocardial Cushion Defects (ASD/VSD). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 40-41. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 171-172. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 92-93. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 168-169.

Question 37: All of the following are methods of cellular adaptation EXCEPT?

A. Atrophy
B. Hyperplasia
C. Hypertrophy
D. Dysplasia (Correct Answer)

Explanation: **Explanation:** **Cellular adaptation** refers to reversible functional and structural changes in cells in response to physiological stress or pathological stimuli [3]. These changes allow the cell to survive and maintain homeostasis in a new environment. **Why Dysplasia is the correct answer:** **Dysplasia** is not a true adaptive process; rather, it is characterized by **disordered growth** and maturation. It involves a loss in the uniformity of individual cells and their architectural orientation. While it can be reversible if the stimulus is removed, it is considered a **pre-neoplastic** condition (a precursor to cancer) rather than a healthy adaptive response to stress [4]. **Analysis of Incorrect Options:** * **Atrophy:** An adaptive response where there is a decrease in cell size and number (via autophagy and apoptosis), leading to a reduced size of the organ [2]. * **Hypertrophy:** An increase in the **size** of cells, resulting in an increase in the size of the organ [1]. It occurs in cells with limited replicative capacity (e.g., cardiac muscle). * **Hyperplasia:** An increase in the **number** of cells in an organ or tissue [1]. It occurs in tissues containing cell populations capable of replication (e.g., breast glandular epithelium during pregnancy). **High-Yield Clinical Pearls for NEET-PG:** * **Metaplasia** is the fourth classic type of cellular adaptation (replacement of one adult cell type with another) [5]. * **Dysplasia vs. Neoplasia:** Dysplasia does not inevitably progress to cancer. If the inciting stimulus (like chronic irritation) is removed, dysplasia may regress [4]. * **Key distinction:** Hypertrophy and Hyperplasia often occur together (e.g., the gravid uterus), but in permanent cells like **Myocardium**, only hypertrophy occurs [1]. * **Atrophy mechanism:** Involves increased protein degradation via the **Ubiquitin-Proteasome pathway** [3]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 85-87. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 90-91. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 47-49. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, p. 49. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 91-92.

Question 38: Which of the following can be used as an immunohistochemical marker for juvenile rhabdomyosarcoma?

A. Neurofilament
B. Desmin (Correct Answer)
C. Vimentin
D. Cytokeratin

Explanation: **Explanation:** **1. Why Desmin is the Correct Answer:** Juvenile rhabdomyosarcoma (including embryonal and alveolar subtypes) is a malignant tumor of **skeletal muscle** origin. **Desmin** is an intermediate filament found in all types of muscle cells (skeletal, cardiac, and smooth). Because rhabdomyosarcoma cells recapitulate various stages of myogenesis, they express muscle-specific markers. While **Myogenin** and **MyoD1** are more specific nuclear markers for rhabdomyosarcoma, **Desmin** is the most commonly used cytoplasmic screening marker to confirm the myogenic lineage of a "small round blue cell tumor." **2. Why Other Options are Incorrect:** * **A. Neurofilament:** This is an intermediate filament specific to **neurons**. It is used as a marker for neuroblastoma or primitive neuroectodermal tumors (PNET), not muscle tumors. * **C. Vimentin:** While vimentin is positive in rhabdomyosarcoma, it is a **non-specific** marker for all mesenchymal cells (including fibroblasts, endothelial cells, and most sarcomas). It lacks the specificity required to diagnose a specific subtype like rhabdomyosarcoma. * **D. Cytokeratin:** This is the hallmark marker for **epithelial cells**. It is used to diagnose carcinomas and is typically negative in rhabdomyosarcoma. **3. NEET-PG High-Yield Pearls:** * **Most Specific Markers:** For rhabdomyosarcoma, **Myogenin (Myf4)** and **MyoD1** are superior to Desmin because they are specific to skeletal muscle differentiation [1]. * **Commonest Site:** The most common site for embryonal rhabdomyosarcoma is the **Head and Neck** (followed by the Genitourinary tract). * **Sarcoma Botryoides:** A variant of embryonal rhabdomyosarcoma found in the vagina of infants, characterized by a "grape-like" appearance and a subepithelial **Cambium layer** [1]. * **Translocation:** Alveolar rhabdomyosarcoma is associated with **t(2;13)** involving the *PAX3-FOXO1* gene. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1224-1225.

Question 39: Annexin V is a marker of?

A. Necrosis
B. Gangrene
C. Aging
D. Apoptosis (Correct Answer)

Explanation: **Explanation:** **Why Apoptosis is the correct answer:** Annexin V is a calcium-dependent phospholipid-binding protein with a high affinity for **Phosphatidylserine (PS)**. In healthy cells, PS is strictly maintained on the inner (cytoplasmic) leaflet of the plasma membrane by the enzyme flippase [1]. One of the earliest features of **apoptosis** is the loss of membrane asymmetry, causing PS to "flip" to the outer leaflet [1]. This serves as an "eat-me" signal for phagocytes [2]. Because Annexin V binds specifically to externalized PS, it is used as a sensitive molecular marker to identify and quantify apoptotic cells via flow cytometry. **Why other options are incorrect:** * **Necrosis:** Unlike apoptosis, necrosis involves early loss of membrane integrity (rupture). While Annexin V may bind to internal PS in necrotic cells, it is not a specific marker for the process itself; instead, dyes like Propidium Iodide (PI) are used to differentiate necrosis from apoptosis. * **Gangrene:** This is a clinical term describing macroscopic tissue death (usually coagulative necrosis with or without superadded putrefaction). It is a late-stage morphological change, not a molecular process identified by Annexin V. * **Aging:** Cellular aging (senescence) is characterized by telomere shortening and the accumulation of metabolic damage (e.g., lipofuscin), not the specific externalization of phosphatidylserine. **High-Yield Pearls for NEET-PG:** * **Flip-Flop Mechanism:** The movement of PS from the inner to the outer leaflet is the hallmark of early apoptosis [1]. * **Phagocytosis:** Externalized PS is recognized by macrophages, ensuring "silent" removal of cells without triggering inflammation [2]. * **Other Markers:** Caspases (executioners), Cytochrome C (intrinsic pathway), and DNA ladders (karyorrhexis) are also high-yield markers for apoptosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 19-20. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 67-69.

Question 40: Jumping genes (transposons) are primarily involved in which of the following biological processes?

A. Gene regulation (Correct Answer)
B. Chromosomal aberrations
C. Gene movement within a genome
D. Gene amplification

Explanation: **Explanation:** **Transposons**, commonly known as **"Jumping Genes,"** are mobile genetic elements that can change their position within a genome [1]. While they are physically capable of moving (Option C), their primary biological significance in modern molecular pathology lies in **Gene Regulation (Option A).** [1] **Why Gene Regulation is Correct:** When a transposon moves, it can insert itself into or near a functional gene. This insertion can act as a molecular switch: 1. **Promoter Activity:** Transposons often carry their own promoter sequences, which can activate nearby genes. 2. **Gene Silencing:** If they insert into an exon or a regulatory region, they can disrupt the reading frame or block transcription, effectively "turning off" the gene. 3. **Epigenetic Modification:** They influence chromatin structure, impacting how genes are expressed in different tissues [1]. **Why other options are incorrect:** * **Option B (Chromosomal Aberrations):** While transposons can occasionally cause deletions or inversions, they are not the *primary* mechanism for major chromosomal aberrations (which usually occur during meiosis/mitosis errors). * **Option C (Gene movement):** This describes the *mechanism* of transposons, but the question asks for the *biological process* they are involved in. In a functional context, movement is the means to the end of regulation. * **Option D (Gene amplification):** This refers to an increase in copy number (e.g., N-myc in Neuroblastoma), which is typically mediated by replication errors, not transposition. **High-Yield Clinical Pearls for NEET-PG:** * **Barbara McClintock:** Discovered transposons in maize (Nobel Prize winner). * **Human Genome:** Nearly 45-50% of the human genome consists of transposon-derived sequences (e.g., **Alu elements**, LINEs) [1]. * **Clinical Relevance:** Transposon insertions are linked to diseases like **Hemophilia A** (Factor VIII mutation) and certain hereditary cancers by disrupting tumor suppressor genes [1]. **Note:** Robbins Pathologic Basis of Disease mentions that over one third of the human genome is composed of these elements and they are specifically implicated in gene regulation [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 14-15.

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