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diff --git a/gnqa/paper2_eval/data/dataset/human/intermediate_files/human_cs_aging_3 b/gnqa/paper2_eval/data/dataset/human/intermediate_files/human_cs_aging_3 new file mode 100644 index 0000000..1d57222 --- /dev/null +++ b/gnqa/paper2_eval/data/dataset/human/intermediate_files/human_cs_aging_3 @@ -0,0 +1,65 @@ +{ + "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": [ + "58c6c8e0-734b-539d-8e50-fd3cb02f650e", + "ee9fd19c-ae3c-5da6-9fcd-264bafc68b55", + "254dda83-4350-5b57-b6e4-638addaf7ce3", + "30fc6495-2cc4-5c3a-9d49-555478243db1", + "630a9f0d-d04f-581b-a9a0-3d2de4fff6fe", + "4c08454a-1c63-52e3-b382-0a33cd46b523", + "5436985c-1a11-544d-b935-fe68ee75a956", + "20ef68d8-5bd7-5ed1-937f-4be14c6ce1b0", + "70332eb3-8348-53b6-abd6-724515f363db", + "48a746ad-a07a-5c53-89dc-3c2768900f0d" + ], + "document_id": [ + "bb774030-2570-5596-b2ab-b8f57ff81086", + "b50a9732-7d01-5d4d-8f33-a9d43dbc7df3", + "e67324c0-474b-5280-8cbc-3778c6c0e5f0", + "fcbbb3ce-6524-50e3-9f8d-c191dc551231", + "4db8c752-c8e2-5f6d-a091-dc4f1d0c48bc", + "cc139813-6771-5434-b948-381291c86509", + "cf24db9a-e013-5780-8b0f-369c56143f29", + "6f3d464d-8df0-560e-b579-942810e1107c", + "815a8b4a-6902-5bb9-87e0-563e1ba7a38a", + "d05e3aba-f8c1-5c5c-afff-679fa14b9a16" + ], + "id": [ + "chatcmpl-ADZVPjiJlVpPgOZJvVtmrRMtG8Eg7", + "dfd32439-5b44-5e43-a85b-6dd58810b9ed", + "c02a78d4-b932-5d71-b183-8b1965fef470", + "fdfc9b00-1bce-5f6b-b20f-c516c7b5448a", + "2258748b-d21f-577b-a1f8-0ba4f61b6e30", + "de267316-5a20-5a54-b22f-30c8e0bf426e", + "31910427-870d-5c8c-846f-d355211c632a", + "ee2ce54b-850a-5d36-8781-f8b23585f97d", + "c48f36fa-a9c7-5b9c-a7d1-26850026f3a3", + "3a15c325-3b6e-54ff-a58a-0e61631ed073", + "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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