{
  "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"
  ],
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    "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?"
}