FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2084969905> ?p ?o ?g. }

• W2084969905 endingPage "222" @default.
• W2084969905 startingPage "215" @default.
• W2084969905 abstract "Neuronal and glial cell death and traumatic axonal injury contribute to the overall pathology of traumatic brain injury (TBI) in both humans and animals. In both head-injured humans and following experimental brain injury, dying neural cells exhibit either an apoptotic or a necrotic morphology. Apoptotic and necrotic neurons have been identified within contusions in the acute post-traumatic period, and in regions remote from the site of impact in the days and weeks after trauma, while degenerating oligodendrocytes and astrocytes have been observed within injured white matter tracts. We review and compare the regional and temporal patterns of apoptotic and necrotic cell death following TBI and the possible mechanisms underlying trauma-induced cell death. While excitatory amino acids, increases in intracellular calcium and free radicals can all cause cells to undergo apoptosis, in vitro studies have determined that neural cells can undergo apoptosis via many other pathways. It is generally accepted that a shift in the balance between pro- and anti-apoptotic protein factors towards the expression of proteins that promote death may be one mechanism underlying apoptotic cell death. The effect of TBI on cellular expression of survival promoting-proteins such as Bcl-2, Bcl-xL, and extracellular signal-regulated kinases, and death-inducing proteins such as Bax, c-Jun N-terminal kinase, tumor-suppressor gene, p53, and the calpain and caspase families of proteases are reviewed. In light of pharmacologic strategies that have been devised to reduce the extent of apoptotic cell death in animal models of TBI, our review also considers whether apoptosis may serve a protective role in the injured brain. Together, these observations suggest that cell death mechanisms may be representative of a continuum between apoptotic and necrotic pathways." @default.
• W2084969905 created "2016-06-24" @default.
• W2084969905 creator A5061860555 @default.
• W2084969905 date "2004-04-01" @default.
• W2084969905 modified "2023-10-14" @default.
• W2084969905 title "Cell Death Mechanisms Following Traumatic Brain Injury" @default.
• W2084969905 cites W1519250999 @default.
• W2084969905 cites W1522782595 @default.
• W2084969905 cites W1530284699 @default.
• W2084969905 cites W1530777667 @default.
• W2084969905 cites W1539967852 @default.
• W2084969905 cites W1568752613 @default.
• W2084969905 cites W1631527540 @default.
• W2084969905 cites W1666499734 @default.
• W2084969905 cites W1920883260 @default.
• W2084969905 cites W1928214158 @default.
• W2084969905 cites W1963523765 @default.
• W2084969905 cites W1963857988 @default.
• W2084969905 cites W1966448447 @default.
• W2084969905 cites W1966558330 @default.
• W2084969905 cites W1967399773 @default.
• W2084969905 cites W1970761811 @default.
• W2084969905 cites W1976385326 @default.
• W2084969905 cites W1978629922 @default.
• W2084969905 cites W1979995768 @default.
• W2084969905 cites W1981140277 @default.
• W2084969905 cites W1982598770 @default.
• W2084969905 cites W1982785786 @default.
• W2084969905 cites W1983502376 @default.
• W2084969905 cites W1984616391 @default.
• W2084969905 cites W1986228861 @default.
• W2084969905 cites W1987110784 @default.
• W2084969905 cites W1987696415 @default.
• W2084969905 cites W1987787017 @default.
• W2084969905 cites W1989846518 @default.
• W2084969905 cites W1991799458 @default.
• W2084969905 cites W1993889646 @default.
• W2084969905 cites W1994150905 @default.
• W2084969905 cites W1994278260 @default.
• W2084969905 cites W1994891112 @default.
• W2084969905 cites W1995595961 @default.
• W2084969905 cites W1997492755 @default.
• W2084969905 cites W1998681909 @default.
• W2084969905 cites W2000057840 @default.
• W2084969905 cites W2001512038 @default.
• W2084969905 cites W2005624865 @default.
• W2084969905 cites W2005856601 @default.
• W2084969905 cites W2008186920 @default.
• W2084969905 cites W2010095588 @default.
• W2084969905 cites W2012370852 @default.
• W2084969905 cites W2012485229 @default.
• W2084969905 cites W2016087991 @default.
• W2084969905 cites W2016332747 @default.
• W2084969905 cites W2016723726 @default.
• W2084969905 cites W2020822328 @default.
• W2084969905 cites W2022248426 @default.
• W2084969905 cites W2022647670 @default.
• W2084969905 cites W2023462313 @default.
• W2084969905 cites W2026672310 @default.
• W2084969905 cites W2026761074 @default.
• W2084969905 cites W2027203046 @default.
• W2084969905 cites W2028292565 @default.
• W2084969905 cites W2028608275 @default.
• W2084969905 cites W2028743642 @default.
• W2084969905 cites W2029247231 @default.
• W2084969905 cites W2029430119 @default.
• W2084969905 cites W2029479814 @default.
• W2084969905 cites W2030201417 @default.
• W2084969905 cites W2031595027 @default.
• W2084969905 cites W2032770280 @default.
• W2084969905 cites W2033624750 @default.
• W2084969905 cites W2035274471 @default.
• W2084969905 cites W2035946777 @default.
• W2084969905 cites W2036142609 @default.
• W2084969905 cites W2036316405 @default.
• W2084969905 cites W2038055601 @default.
• W2084969905 cites W2040053768 @default.
• W2084969905 cites W2041391753 @default.
• W2084969905 cites W2043033966 @default.
• W2084969905 cites W2044704316 @default.
• W2084969905 cites W2045086385 @default.
• W2084969905 cites W2048608744 @default.
• W2084969905 cites W2059006262 @default.
• W2084969905 cites W2060911909 @default.
• W2084969905 cites W2061497413 @default.
• W2084969905 cites W2062868334 @default.
• W2084969905 cites W2068050476 @default.
• W2084969905 cites W2069359956 @default.
• W2084969905 cites W2069824337 @default.
• W2084969905 cites W2070673299 @default.
• W2084969905 cites W2070719568 @default.
• W2084969905 cites W2076392120 @default.
• W2084969905 cites W2076825885 @default.
• W2084969905 cites W2082259697 @default.
• W2084969905 cites W2084959937 @default.
• W2084969905 cites W2085013961 @default.
• W2084969905 cites W2085459880 @default.
• W2084969905 cites W2089691927 @default.

• next