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+{
+  "titles": [
+    "2020 - Protecting the Aging Genome.pdf",
+    "2013 - Pathways, Networks and Systems Medicine Conferences.pdf",
+    "2012 - Pleiotropic Cellular Functions of PARP1 in Longevity.pdf",
+    "2008 - Biotools for Determining the Genetics of Susceptibility to Infectious Diseases.pdf",
+    "2008 - (Infectious Disease) Karl A. Western (auth.), Vassil St. Georgiev PhD, Karl A. Western MD, John J. McGowan PhD (eds.) - National Institute of Allergy and Infectious Diseases, NIH_ Frontiers in Researc (3).pdf",
+    "1999 - The NOD mouse model of type 1 diabetes.pdf",
+    "2012 - Genome-Wide Analysis of Yeast Aging.pdf",
+    "2005 -Liang- GENETIC REGULATION OF HEMATOPOIETIC STEM CELL NUMBERS IN MICE.pdf",
+    "2005 - GENETIC REGULATION OF HEMATOPOIETIC STEM CELL NUMBERS IN MICE.pdf",
+    "2006 - Molecular pathogenesis of thyroid cancer the significance.pdf"
+  ],
+  "extraction_id": [
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+  "document_id": [
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+    "fe4906aa-37b1-5514-962c-1e8dc5b2fb13"
+  ],
+  "contexts": [
+    "Cell Death A form of programmed cell death, apoptosis is necessary for normal cell turnover and is essential to a plethora of other biological processes. Apoptosis can be executed via Bcl-2 activation of caspases, via signals from the death receptor on the plasma membrane, or via induction by granzyme Bsecreted from cytotoxic T cells (Tc cells) [ 35]. Endonucleases and proteases are activated by active caspases, eventually leading to the death of the cell. With age, however, apoptotic activity changes.",
+    "(during development and for maintenance of homeostasis) in multi -cellular  organism is apoptosis, which is character ized by a  sequence of well -defined  events resulting in cell destruction. Dysregulation of apoptosis is responsible for  many physiological health problems and diseases; therefore, it is necessary to  understand  the responsible signaling pathways and complex interplay of  cellularprocesses. Results:   A combined mathematical model of apoptosis",
+    "is, apoptosis and necrosis. Apoptosis is considered as thedefault pathway, where cell death occurs in a controlledmanner resulting in the elimination of cells by macrophageswithout secondary damage of the surrounding cells. In con-trast, necrosis is considered an uncontrolled process whichleads to disruption of cells promoting tissue inammation[187]. Several transition states between the two pathways",
+    "tion of cells undergoing apoptosis.   Immunol Today   14:  131  136.       82.     Platt   N,     Silva   RP,   da    Gordon   S    (1998)   Recognizing death: the  phagocytosis of apoptotic cells.   Trends Cell Biol   8:  365  372.       83.     Giles   KM,     Hart   SP,     Haslett   C,     Rossi   AG,     Dransfield   I    (2000)    An appetite for apoptotic cells? Controversies and challenges.    Br J Haematol   109:  1  12.",
+    "tion of cells undergoing apoptosis.   Immunol Today   14:  131  136.       82.     Platt   N,     Silva   RP,   da    Gordon   S    (1998)   Recognizing death: the  phagocytosis of apoptotic cells.   Trends Cell Biol   8:  365  372.       83.     Giles   KM,     Hart   SP,     Haslett   C,     Rossi   AG,     Dransfield   I    (2000)    An appetite for apoptotic cells? Controversies and challenges.    Br J Haematol   109:  1  12.",
+    "the induc-tion of apoptosis.",
+    "to cancer , b ut probably not rele v ant to the i ntrinsic aging process i n yeast. Apoptosis Cell suicide, or apoptosis, i s a well-studied biological phenomenon in multicellular or g anisms t hat allo ws specic cells to be remo v e d during t he de v e lopment of com- ple x tissues, o r potentially dangerous damaged cells to be destro yed for t he benetof the w hole o r g anism. T he lack of an apparent e v olutionary benet for s uch a p ro-",
+    "15Apoptosis is caused by the activation of the caspase cascade, which isinitiated by two signaling routes (stress-induced death and death-domainreceptor-induced death) (Domen 2001). This process can be prevented by anti-apoptotic molecules, such as Bcl-2 (Domen and Weissman 2000). Directevidence for the involvement of apoptosis in HSC number regulation came fromthe findings that overexpression of the anti-apoptotic gene bcl-2 led to increasednumbers of Thy-1.1low, Sca-1+, c-kit+, Lin- cells, a population",
+    "15Apoptosis is caused by the activation of the caspase cascade, which isinitiated by two signaling routes (stress-induced death and death-domainreceptor-induced death) (Domen 2001). This process can be prevented by anti-apoptotic molecules, such as Bcl-2 (Domen and Weissman 2000). Directevidence for the involvement of apoptosis in HSC number regulation came fromthe findings that overexpression of the anti-apoptotic gene bcl-2 led to increasednumbers of Thy-1.1low, Sca-1+, c-kit+, Lin- cells, a population",
+    "Apoptosis modulating genesApopotosis or programmed cell death is associated withalterations in cell morphology, particularly the nucleus, withendonucleatytic cleavage of DNA into nucleosomal lengthfragments.Apoptosis may resultfrom withdrawalofgrowth signals.Fas, a transmembrane protein of the nerve growth factor/tumor necrosis factor receptor family signals apoptotic de-ath signals apoptotic death in some cell types. Fas but notbel-2 gene expression is negatively regulated by TSH (Ka-wakami et al., 1996),"
+  ],
+  "answer": "Apoptosis is a form of programmed cell death that is essential for normal cell turnover and various biological processes [1]. It is characterized by a sequence of well-defined events leading to cell destruction [2]. Apoptosis occurs in a controlled manner, resulting in the elimination of cells by macrophages without causing secondary damage to surrounding cells [3]. This process can be initiated through several pathways, including Bcl-2 activation of caspases, signals from death receptors on the plasma membrane, or induction by granzyme B secreted from cytotoxic T cells [1].",
+  "question": "What is apoptosis?"
+}
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