Kasra Khalaj

31 timestamped statements across 1 collection — auto-found in recorded discussions, each timestamp jumps to the exact moment.

Featured diaries

▶ Ep 8 · 1:55
Many refer to autophagy as a recycling mechanism of cellular tra, so to speak, and this is because it's one of the key ways that cell survival is promoted.
quote · Congenital Diaphragmatic Hernia
▶ Ep 8 · 0:31
It is well known that hypoplastic lungs of babies with pulmonary hypoplasia secondary to CDH have impaired fetal lung growth and maturation.
quote · Congenital Diaphragmatic Hernia

Nothing matches these filters — clear the search or widen the filters.

Congenital Diaphragmatic Hernia 31 entries

EUPSA - MicroRNAs in amniotic fluid stem cellextracellular vesicles modulate lung development in experimental congenital diaphragmatic hernia - Kasra Khalaj

▶ Ep 8 · 0:31
clinical Hypoplastic lungs of babies with pulmonary hypoplasia secondary to CDH have impaired fetal lung growth and maturation ↗
▶ Ep 8 · 0:31
quote It is well known that hypoplastic lungs of babies with pulmonary hypoplasia secondary to CDH have impaired fetal lung growth and maturation. ↗
▶ Ep 8 · 0:39
clinical Several treatment agents have been administered prenatally for CDH, but none have been shown to fully rescue lung development ↗
▶ Ep 8 · 0:45
clinical Extracellular vesicles are nanoparticles known to be the mediators of stem cell paracrine signaling ↗
▶ Ep 8 · 0:56
clinical AFSCEV administration rescued the number of lung branches back to normal in CDH models ↗
▶ Ep 8 · 1:07
clinical AFSCEVs improve fetal lung maturation as shown by rescuing the expression of surfactant protein C ↗
▶ Ep 8 · 1:17
clinical AFSCEVs contain microRNA 17-92 cluster, which has been reported in the literature to modulate fetal lung development ↗
▶ Ep 8 · 1:31
clinical Knockout of the microRNA 17-92 cluster can recapitulate pulmonary hypoplasia ↗
▶ Ep 8 · 1:46
clinical Autophagy has been shown to be critical for lung branching morphogenesis ↗
▶ Ep 8 · 1:55
clinical Autophagy is a recycling mechanism of cellular trash and is one of the key ways that cell survival is promoted ↗
▶ Ep 8 · 1:55
quote Many refer to autophagy as a recycling mechanism of cellular tra, so to speak, and this is because it's one of the key ways that cell survival is promoted. ↗
▶ Ep 8 · 2:04
clinical Autophagy is most impaired at the pseudoglandular and canalicular stages in the nitrofen model of CDH ↗
▶ Ep 8 · 2:18
clinical High levels of sequestosome indicate autophagy impairment ↗
▶ Ep 8 · 2:18
clinical CDH fetal lungs show reduced levels of Beclin 1 and ATG5 (autophagy activators) and higher levels of sequestosome (autophagy adapter) at pseudoglandular and canalicular stages ↗
▶ Ep 8 · 2:32
clinical Treatment with AFSCEVs restores autophagy key genes (Beclin 1, ATG5, sequestosome) at the pseudoglandular and canalicular stage ↗
▶ Ep 8 · 2:56
clinical AFSCEVs are taken up by virtually all cells in fetal lung explants, including the fetal lung epithelium ↗
▶ Ep 8 · 3:19
clinical Activation of autophagy by AFSCEVs is localized in the lung epithelial compartment of the fetal lung microenvironment ↗
▶ Ep 8 · 3:27
clinical Knockdown of microRNAs 17 and 20 in AFSCEVs results in increased sequestosome and down regulation of Beclin mRNA, indicating impaired autophagy ↗
▶ Ep 8 · 3:53
clinical Knockdown of microRNAs 17 and 20 results in lower levels of LC3B2 protein, which is the active isoform of the autophagy cascade ↗
▶ Ep 8 · 4:03
quote Well, by now I bet you're all asking, well, are these findings clinically relevant in human CDH? ↗
▶ Ep 8 · 4:10
clinical Human fetal lung explant model of pulmonary hypoplasia was established using fetal lungs from healthy terminated fetuses from 15 to 19 weeks of gestation, corresponding to late pseudoglandular and canalicular stages ↗
▶ Ep 8 · 4:37
clinical In human hypoplastic fetal lung explants, there is a reduction of Beclin 1 and ATG5 at the mRNA level ↗
▶ Ep 8 · 4:58
clinical Treatment with human AFSCEVs results in restoration of Beclin 1 and ATG5 in human hypoplastic fetal lung explants ↗
▶ Ep 8 · 5:04
clinical At the protein level in human tissue, all three autophagy markers (Beclin 1, ATG5, sequestosome) were dysregulated in the hypoplastic group, and human AFSCEVs restored all three markers back to control ↗
▶ Ep 8 · 5:17
quote In conclusion, we are very excited as this is the first study discovering an important mechanism in the CDH pathophysiology. ↗
▶ Ep 8 · 5:17
opinion This is the first study discovering autophagy impairment as an important mechanism in CDH pathophysiology ↗
▶ Ep 8 · 5:24
clinical Autophagy levels are restored with administration of AFSCEVs, thus partially explaining their effect on branching morphogenesis ↗
▶ Ep 8 · 5:31
clinical Autophagy can be targeted with microRNAs 17 and 20 ↗
▶ Ep 8 · 7:39
opinion Future work includes looking at ER stress, which is very closely interrelated with autophagy pathway, to see if AFSCEVs can exert an effect on this related mechanism ↗
▶ Ep 8 · 8:07
clinical Studies in oncology have shown that the quantity of extracellular vesicles released when autophagy is impaired is different ↗
▶ Ep 8 · 8:37
opinion Future functional studies will examine endogenous extracellular vesicle production in hypoplastic fetal lungs ↗