General Pathology — MCQs
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In Xeroderma Pigmentosum, which DNA repair pathway is defective?
What is the pathophysiology of Chronic Granulomatous disease?
A 30-year-old woman suffers a traumatic injury to her breast while playing soccer. Physical examination reveals a 3-cm area of ecchymosis on the left breast. Two weeks later, the patient palpates a firm lump beneath the area where the bruise had been located. Which of the following is the most likely pathologic diagnosis?
DNA integrity and replication are ensured at which stage of the cell cycle?
Which of the following findings is not compatible with a diagnosis of juvenile myelomonocytic leukemia?
Which of the following is NOT a granulomatous disease?
Which of the following is a characteristic of classical Mendelian inheritance of an autosomal dominant disease?
What is true about Malacetic teeth?
Thistle-tube appearance is a characteristic feature of which condition?
Which of the following is referred to as the "Governor of Proliferation"?
General Pathology Indian Medical PG Practice Questions and MCQs
Question 241: In Xeroderma Pigmentosum, which DNA repair pathway is defective?
- A. Base pair defect
- B. Nucleotide Excision Repair (Correct Answer)
- C. Mismatch repair defect
- D. Protein folding
Explanation: **Explanation:** **Nucleotide Excision Repair (NER)** is the correct answer because Xeroderma Pigmentosum (XP) is an autosomal recessive disorder characterized by an inherited deficiency in the enzymes required for this specific pathway. NER is responsible for identifying and removing bulky DNA lesions, most notably **pyrimidine dimers** (thymine dimers) caused by exposure to **Ultraviolet (UV) radiation** [1]. When this pathway is defective, DNA damage accumulates, leading to extreme photosensitivity and a 2000-fold increased risk of skin cancers (Basal Cell Carcinoma, Squamous Cell Carcinoma, and Melanoma) [1]. **Analysis of Incorrect Options:** * **Option A (Base Excision Repair):** This pathway repairs non-bulky damage (e.g., deamination or oxidized bases) using glycosylases. It is not the primary defect in XP. * **Option C (Mismatch Repair):** Defects in this pathway (MLH1, MSH2) lead to **Lynch Syndrome** (Hereditary Non-Polyposis Colorectal Cancer) and are characterized by microsatellite instability. * **Option D (Protein Folding):** This refers to proteostasis issues (e.g., Amyloidosis or Prion diseases) and is unrelated to DNA repair mechanisms. **High-Yield Clinical Pearls for NEET-PG:** * **Key Enzyme:** The most common defect involves **UV-specific endonuclease**. * **Clinical Presentation:** "Sunburn on first exposure," severe freckling (lentigines) before age 2, and progressive neurological degeneration in some subtypes (De Sanctis-Cacchione syndrome). * **Associated Cancers:** Early-onset skin cancers and internal malignancies [1]. * **Diagnosis:** Chromosomal breakage studies or unscheduled DNA synthesis (UDS) assays. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 322-323.
Question 242: What is the pathophysiology of Chronic Granulomatous disease?
- A. Defective myeloperoxidase
- B. Decreased oxidative burst (Correct Answer)
- C. Impaired phagocytosis
- D. Impaired activity of lysozyme
Explanation: **Explanation:** **Chronic Granulomatous Disease (CGD)** is a primary immunodeficiency caused by a genetic defect in the **NADPH oxidase enzyme complex** within phagocytes (neutrophils and macrophages). 1. **Why Option B is correct:** NADPH oxidase is responsible for converting molecular oxygen into superoxide radicals ($O_2^-$) [1]. This process is known as the **Respiratory (Oxidative) Burst**. In CGD, the absence of this enzyme leads to a failure in producing reactive oxygen species (ROS) like superoxide and hydrogen peroxide. Consequently, phagocytes can ingest bacteria but cannot kill them, leading to persistent infections and the formation of granulomas. 2. **Why other options are incorrect:** * **Option A:** Myeloperoxidase (MPO) deficiency is a separate condition where patients cannot convert $H_2O_2$ to $HOCl$ (bleach) [1]. While it affects killing, the oxidative burst itself is intact. * **Option C:** Phagocytosis (the ingestion of microbes) is normal in CGD; the defect lies in the intracellular killing mechanism [1]. * **Option D:** Lysozymes are hydrolytic enzymes in granules [2]. CGD specifically affects the oxidative pathway, not the enzymatic degranulation process. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most common is **X-linked recessive** (CYBB gene mutation). * **Organisms:** Patients are susceptible to **Catalase-positive organisms** (e.g., *Staphylococcus aureus*, *Aspergillus*, *Nocardia*, *Serratia marcescens*, and *Burkholderia cepacia*). Catalase-positive bugs neutralize their own $H_2O_2$, leaving the deficient neutrophil with no ROS to use. * **Diagnostic Tests:** * **Nitroblue Tetrazolium (NBT) test:** Negative (remains colorless/yellow; does not turn blue). * **Dihydrorhodamine (DHR) Flow Cytometry:** Most sensitive/specific (shows decreased fluorescence). This is now the gold standard. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 91. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 91-92.
Question 243: A 30-year-old woman suffers a traumatic injury to her breast while playing soccer. Physical examination reveals a 3-cm area of ecchymosis on the left breast. Two weeks later, the patient palpates a firm lump beneath the area where the bruise had been located. Which of the following is the most likely pathologic diagnosis?
- A. Duct ectasia
- B. Fat necrosis (Correct Answer)
- C. Fibrocystic change
- D. Granulomatous mastitis
Explanation: **Explanation:** **Why Fat Necrosis is correct:** The clinical scenario describes a classic presentation of **Fat Necrosis of the breast**. This condition typically follows physical trauma (like a sports injury) or surgery. The underlying mechanism involves the release of fatty acids from damaged adipocytes, which triggers an inflammatory response. Over time, this leads to fibrosis and the formation of a **firm, painless, palpable lump** that can clinically mimic breast carcinoma. Histologically, it is characterized by "ghost cells" (necrotic adipocytes without nuclei), lipid-laden macrophages (foam cells), and eventually calcification. **Why the other options are incorrect:** * **A. Duct ectasia:** This is an inflammatory condition involving the dilation of large subareolar ducts, typically seen in older, multiparous women [1]. It usually presents with nipple discharge (green/brown) rather than a post-traumatic lump [1]. * **C. Fibrocystic change:** This is a common, benign condition characterized by cyclic breast pain (mastalgia) and "lumpy" breasts that fluctuate with the menstrual cycle [2]. It is not associated with acute trauma [2]. * **D. Granulomatous mastitis:** This is a rare inflammatory condition often associated with systemic diseases (like Sarcoidosis or TB) or idiopathic causes (post-pregnancy). It presents with chronic inflammation and abscesses, not typically triggered by a single traumatic event. **NEET-PG High-Yield Pearls:** * **Clinical Mimicry:** Fat necrosis is high-yield because it can mimic breast cancer both on physical exam (firm, fixed mass) and mammography (irregular mass with calcifications). * **Saponification:** The release of fatty acids and their reaction with calcium leads to **dystrophic calcification**, a process known as saponification. * **Key Histology:** Look for "anucleated adipocytes" and "foreign body giant cell reaction" in biopsy descriptions. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1050-1052. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, p. 1052.
Question 244: DNA integrity and replication are ensured at which stage of the cell cycle?
- A. End of M
- B. End of G1
- C. End of S
- D. End of G2 (Correct Answer)
Explanation: **Explanation:** The cell cycle is governed by specific "checkpoints" that ensure the fidelity of DNA before the cell proceeds to the next phase [1]. **Why the correct answer is D (End of G2):** The **G2/M checkpoint** (at the end of G2) is the critical regulatory step where the cell ensures that **DNA replication is complete** and any **DNA damage is repaired** before entering Mitosis (M phase) [1]. This prevents the propagation of mutations or chromosomal aberrations to daughter cells. This checkpoint is primarily regulated by the **Cyclin B-CDK1 complex** (also known as Mitosis-Promoting Factor or MPF). **Analysis of Incorrect Options:** * **A. End of M:** The checkpoint here (Spindle Checkpoint) ensures that all chromosomes are properly attached to the spindle fibers before anaphase, rather than checking DNA replication integrity. * **B. End of G1:** This is the "Restriction Point." It checks for cell size, nutrients, and DNA damage *before* replication begins in the S phase [1], [2]. It does not ensure replication integrity as replication hasn't occurred yet. * **C. End of S:** While there are intra-S phase checkpoints to monitor replication stress, the final "quality control" and verification of completed replication occur at the end of G2. **Clinical Pearls for NEET-PG:** * **p53 (The Guardian of the Genome):** Plays a vital role at the G1/S checkpoint by inducing p21, which inhibits CDKs and halts the cycle to allow for DNA repair [2]. * **G1/S Checkpoint:** Most critical for cell cycle commitment; once passed, the cell usually completes the cycle [1]. * **G2/M Checkpoint:** Most critical for ensuring **DNA integrity** post-replication [1]. * **Ataxia-Telangiectasia:** Caused by a mutation in the *ATM* gene, which is essential for the G2/M checkpoint response to double-stranded DNA breaks. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 37-38. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 302-303.
Question 245: Which of the following findings is not compatible with a diagnosis of juvenile myelomonocytic leukemia?
- A. Peripheral blood monocytosis, more than 1 x 10^9/L
- B. Increased hemoglobin F levels for age
- C. Presence of bcr/abl fusion gene (Correct Answer)
- D. GM-CSF hypersensitivity of myeloid progenitors in vitro
Explanation: **Explanation:** Juvenile Myelomonocytic Leukemia (JMML) is a unique, aggressive clonal hematopoietic stem cell neoplasm of childhood that overlaps features of both myelodysplastic and myeloproliferative syndromes. **Why Option C is the correct answer:** The hallmark of JMML is the **absence of the Philadelphia chromosome ($t(9;22)$) or the $BCR/ABL1$ fusion gene** [1]. The presence of $BCR/ABL1$ is diagnostic of Chronic Myeloid Leukemia (CML), which is extremely rare in children [2]. JMML is instead characterized by mutations in the **RAS signaling pathway** (including *PTPN11*, *NF1*, *NRAS*, *KRAS*, or *CBL* mutations) in approximately 90% of patients. **Analysis of Incorrect Options:** * **Option A:** Absolute peripheral blood **monocytosis (>1 x 10⁹/L)** is a mandatory diagnostic criterion for JMML. * **Option B:** Elevated **Hemoglobin F (HbF)** levels for age are found in about 75% of JMML cases, reflecting the "fetal" or primitive nature of the malignant clone. * **Option D:** Spontaneous growth or **hypersensitivity to Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF)** in colony assays is a classic laboratory feature of JMML and serves as a major diagnostic criterion. **NEET-PG High-Yield Pearls:** * **Age Group:** Typically affects children <3 years old. * **Clinical Presentation:** Hepatosplenomegaly, lymphadenopathy, and skin rashes (xanthomas or café-au-lait spots). * **Association:** Strongly associated with **Neurofibromatosis Type 1 (NF1)** and **Noonan Syndrome**. * **Blast Count:** Blasts in the blood and bone marrow must be **<20%** (otherwise, it is classified as Acute Leukemia) [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 624. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 625-626.
Question 246: Which of the following is NOT a granulomatous disease?
- A. Leprosy
- B. Tuberculosis
- C. Sarcoidosis
- D. Amebiasis (Correct Answer)
Explanation: **Explanation:** A **granuloma** is a distinctive pattern of chronic inflammation characterized by a focal collection of activated macrophages, which often transform into **epithelioid cells**, surrounded by a collar of lymphocytes and occasionally plasma cells [2]. **Why Amebiasis is the correct answer:** Amebiasis, caused by the protozoan *Entamoeba histolytica*, typically results in **liquefactive necrosis** and acute inflammatory responses. In the colon, it produces classic "flask-shaped ulcers," and in the liver, it causes "anchovy sauce" pus abscesses [1]. It does not trigger the Type IV hypersensitivity reaction required to form organized granulomas. **Analysis of incorrect options:** * **Tuberculosis:** The prototype of granulomatous disease [4]. It features **caseating granulomas** (central cheesy necrosis) and Langhans giant cells [3]. * **Leprosy:** Caused by *Mycobacterium leprae*. Tuberculoid leprosy presents with well-formed non-caseating granulomas, while lepromatous leprosy shows foamy macrophages (Virchow cells) due to a poor T-cell response. * **Sarcoidosis:** A multisystem disease of unknown etiology characterized by **non-caseating granulomas** [2]. A key histological feature is the presence of **Schaumann bodies** and **Asteroid bodies** within giant cells. **NEET-PG High-Yield Pearls:** 1. **Epithelioid cells** are the hallmark of a granuloma; they are modified macrophages with abundant pink cytoplasm [2]. 2. **Non-caseating granulomas** are also seen in Crohn’s disease, Cat-scratch disease (stellate shape), and Berylliosis [2]. 3. **Caseating granulomas** are primarily seen in Tuberculosis and certain fungal infections (e.g., Histoplasmosis) [4]. 4. **Schistosomiasis** is a classic parasitic cause of granulomas (reaction to eggs), unlike Amebiasis. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 364-365. [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. 198-200. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 363-364. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 360.
Question 247: Which of the following is a characteristic of classical Mendelian inheritance of an autosomal dominant disease?
- A. Complete penetrance
- B. Affected individuals have unaffected parents
- C. Very early onset in life
- D. Variable expressivity (Correct Answer)
Explanation: **Explanation:** Autosomal dominant (AD) disorders are characterized by the inheritance of a single mutant allele that is sufficient to cause the disease [3]. **1. Why "Variable Expressivity" is correct:** In AD disorders, individuals with the same genotype (the same mutation) can show a wide range of clinical severity or different clinical features. This is known as **variable expressivity**. For example, in Neurofibromatosis Type 1, one patient may only have café-au-lait spots, while their sibling may have extensive neurofibromas and skeletal deformities. **2. Why other options are incorrect:** * **A. Complete penetrance:** Many AD disorders exhibit **reduced (incomplete) penetrance**, where an individual inherits the mutant gene but does not express the phenotype at all [1]. * **B. Affected individuals have unaffected parents:** This describes Autosomal Recessive inheritance [3]. In AD inheritance, every affected person usually has at least one affected parent (unless it is a *de novo* mutation). * **C. Very early onset in life:** AD disorders often have a **delayed onset** (e.g., Huntington’s disease or Adult Polycystic Kidney Disease), whereas Autosomal Recessive disorders typically manifest early in childhood [2]. **NEET-PG High-Yield Pearls:** * **Pleiotropy:** A single gene mutation leading to multiple, seemingly unrelated phenotypic effects (e.g., Marfan syndrome affecting eyes, heart, and skeleton). * **Dominant Negative Effect:** When a mutant protein impairs the function of the normal protein produced from the wild-type allele (common in Collagen disorders). * **Anticipation:** Increased severity or earlier onset in successive generations, typically seen in triplet repeat expansion disorders like Huntington’s. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, p. 147. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 149-150. [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. 53-54.
Question 248: What is true about Malacetic teeth?
- A. These are soft teeth.
- B. Softness is due to an increased amount of interglobular dentin.
- C. This softness leads to increased susceptibility to caries.
- D. All of the above. (Correct Answer)
Explanation: **Explanation:** **Malacetic teeth** (also known as "Mala-acetic" or "Malacic" teeth) refer to a specific dental pathology characterized by defective mineralization of the dentin. 1. **Pathophysiology (Why the answer is correct):** The core defect in malacetic teeth is the failure of calcification of the dentin matrix. Under normal conditions, dentin mineralizes through the fusion of small calcified globules (calcospherites). In this condition, these globules fail to fuse properly, leaving unmineralized spaces known as **interglobular dentin**. 2. **Structural Integrity:** Because the interglobular spaces lack hydroxyapatite, the overall structure of the tooth becomes significantly **softer** than normal healthy teeth. 3. **Clinical Consequence:** The presence of increased interglobular dentin creates a porous, less dense environment. This structural weakness makes the teeth highly **susceptible to dental caries**, as the softened matrix allows for faster acid demineralization and bacterial penetration. **Analysis of Options:** * **Option A & B:** These are correct as they describe the physical state (softness) and the histological cause (interglobular dentin). * **Option C:** This is correct as it describes the primary clinical complication resulting from the structural defect. * **Option D:** Since all individual statements are pathologically linked, "All of the above" is the correct choice. **High-Yield Pearls for NEET-PG:** * **Interglobular Dentin:** Usually found in the circumpulpal dentin, just below the mantle dentin. It is a hallmark of Vitamin D deficiency (Rickets) and systemic fluoride toxicity. * **Clinical Correlation:** Malacetic teeth are frequently associated with **Rickets** due to the systemic lack of calcium and phosphate required for proper dentin globule fusion [1], [2]. * **Contrast:** Do not confuse this with *Amelogenesis Imperfecta*, which primarily affects the enamel, whereas malacetic teeth involve a dentin mineralization defect. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 666-667. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Central Nervous System Synapse, pp. 448-449.
Question 249: Thistle-tube appearance is a characteristic feature of which condition?
- A. Radicular dentin dysplasia
- B. Coronal dentin dysplasia (Correct Answer)
- C. Amelogenesis imperfecta
- D. Dentinogenesis imperfecta
Explanation: **Explanation:** The **thistle-tube appearance** is a classic radiographic hallmark of **Coronal Dentin Dysplasia (Dentin Dysplasia Type II)**. In this autosomal dominant condition, the primary teeth typically appear opalescent (similar to dentinogenesis imperfecta), but the permanent teeth have a normal clinical color. Radiographically, the pulp chambers of the permanent teeth are abnormally large and elongated, extending apically to resemble a **thistle-tube** or flame shape, often containing multiple pulp stones. **Analysis of Options:** * **Coronal Dentin Dysplasia (Type II):** Characterized by the thistle-tube pulp chamber in permanent teeth and obliterated pulp in primary teeth. * **Radicular Dentin Dysplasia (Type I):** Known as "rootless teeth." Radiographs show short, blunted, or conical roots with total pulp obliteration, resulting in a **half-moon/crescent-shaped** pulp remnant. * **Amelogenesis Imperfecta:** A defect primarily affecting **enamel** formation (ectodermal). Dentin and pulp chambers usually appear normal, though enamel may be thin or absent. * **Dentinogenesis Imperfecta:** Characterized by early, total **obliteration of pulp chambers** and canals in both dentitions, along with "bulbous" crowns and cervical constriction (bell-shaped crowns). **NEET-PG High-Yield Pearls:** * **Dentin Dysplasia Type I:** "Rootless teeth" + Crescent-shaped pulp. * **Dentin Dysplasia Type II:** "Thistle-tube" pulp + Pulp stones. * **Dentinogenesis Imperfecta:** Bulbous crowns + Obliterated pulp + Shell teeth (in Type III). * **Regional Odontodysplasia:** "Ghost teeth" appearance (thin enamel and dentin).
Question 250: Which of the following is referred to as the "Governor of Proliferation"?
- A. RB (Correct Answer)
- B. TP53
- C. APC
- D. Patched
Explanation: The correct answer is **A. RB (Retinoblastoma Gene)**. ### **Explanation** The **RB gene**, located on chromosome **13q14** [4], is famously termed the **"Governor of Proliferation"** [1] because it acts as a critical gatekeeper of the cell cycle. Its primary function is to control the **G1 to S phase transition** [2]. * **Mechanism:** In its **hypophosphorylated (active)** state, the RB protein binds to and sequesters the **E2F transcription factor**, preventing the cell from entering the S phase [1]. When the cell receives growth signals, Cyclin D-CDK4/6 complexes **hyperphosphorylate (inactivate)** RB, releasing E2F and allowing DNA replication to proceed [1],[2]. Loss of RB function removes this "brake," leading to uncontrolled cell division. ### **Why other options are incorrect:** * **B. TP53:** Known as the **"Guardian of the Genome"** [1]. It monitors DNA damage and induces cell cycle arrest (via p21), DNA repair, or apoptosis [3]. It does not "govern" the normal proliferative cycle in the same way RB does. * **C. APC:** Known as the **"Gatekeeper of Colonic Neoplasia."** It regulates the WNT signaling pathway by promoting the degradation of β-catenin. * **D. Patched (PTCH):** A tumor suppressor gene involved in the **Hedgehog signaling pathway**. Mutations are associated with Gorlin Syndrome (Basal Cell Nevus Syndrome). ### **High-Yield NEET-PG Pearls:** * **Knudson’s Two-Hit Hypothesis:** Originally described for RB; both alleles must be inactivated for tumor formation [4]. * **Associated Tumors:** Germline mutations lead to familial Retinoblastoma and **Osteosarcoma**. * **Viral Interaction:** Human Papillomavirus (HPV) **E7 protein** binds and inactivates RB, while **E6** inactivates p53 [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 301-302. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 300-301. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 302-303. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 300.
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