Increased apoptosis in the cingulate sulcus of newborn piglets following transient hypoxia-ischaemia is related to the degree of high energy phosphate depletion during the insult
References (8)
- et al.
In situ end-labelling detects DNA strand breaks in apoptosis and other physiological and pathological states
J. Pathol.
(1993) - et al.
Prognosis of newborn infants with hypoxic-ischemic brain injury assessed by phosphorus magnetic resonance spectroscopy
Pediatr. Res.
(1989) - Lorek, A., Takei, Y., Cady, E.B., Wyatt, J.S., Penrice, J., Edwards, A.D., Peebles, D.M., Wylezinska, M., Owen-Rees,...
Social controls on cell survival and cell death
Nature
(1992)
Cited by (122)
A stabilized retro-inverso peptide ligand of transferrin receptor for enhanced liposome-based hepatocellular carcinoma-targeted drug delivery
2019, Acta BiomaterialiaCitation Excerpt :Slight weight gain in some groups might be due to the tumor growth. Apoptosis and necrosis of cells could be preliminarily observed histologically by H&E staining [45]. To better evaluate the apoptosis and necrosis of tumors, tumor tissues were also evaluated qualitatively for Caspase 3 by immunohistochemistry.
Behavioral benefits of maternal swimming are counteracted by neonatal hypoxia-ischemia in the offspring
2016, Behavioural Brain ResearchCitation Excerpt :Considering that we evaluated only a specific time-point, collecting the samples after the memory task, we possibly missed the effect of maternal exercise on BDNF, and observe only the effect from behavioral task, which clearly increases BDNF levels associated with learning test [67–69]. In addition, some studies have shown that this neurotrophic factor protects against injuries caused by HI [46,70–73], being indicated even as a possible treatment against CNS damage. In summary, maternal exercise enhances recognition memory in a BDNF-independent pathway, a positive effect restricted to adult male offspring; highlighting the intrauterine metabolic programming that occurs in the fetuses and its long-lasting effects extended to the adulthood.
Cortical structural abnormalities in very preterm children at 7years of age
2015, NeuroImageCitation Excerpt :The mechanism responsible for this alteration in cingulate sulcal structure remains unknown, but if cortical folding is driven by mechanical tension along long-distance axons (Van Essen, 1997), folding abnormalities may reflect altered patterns of connectivity in VPT children. This is consistent with the observation that hypoxia–ischemia, a known risk factor for brain injury in preterm infants (Dammann and Leviton, 1997; Greisen and Vannucci, 2001), produces an increased number of apoptotic cingulate neurons in piglets (Mehmet et al., 1994). The asymmetry of sulcal abnormalities in our findings are consistent with previous reports of anatomical asymmetries in medial cortical regions (Paus et al., 1996a,1996b; Thompson et al., 2010).
Apoptotic Cell Death
2011, Fetal and Neonatal Physiology E-Book, Fourth EditionThe Discovery of Hypothermic Neural Rescue Therapy for Perinatal Hypoxic-Ischemic Encephalopathy
2009, Seminars in Pediatric Neurology