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Tien Manh Huynh,Quang Dinh Le,Mai Ngoc Luu,Tram Thi Huyen Nguyen,Quy Nhuan Bui,Anh Phan Tuong Mai,Thang Hiep Duc Tran,Hien Minh Tran,Cong Hong Minh Vo,Duc Trong Quach 소화기인터벤션의학회 2022 Gastrointestinal Intervention Vol.11 No.3
Jejunal Dieulafoy lesion (DL) is an exceedingly rare, life-threatening cause of gastrointestinal bleeding. Due to its rarity, intermittent bleeding symptoms that often necessitate prompt clinical intervention, variability in detection and treatment methods, and the risk of rebleeding, this condition frequently presents a diagnostic and therapeutic conundrum. We report a case of severe, intermittent, recurrent hematochezia due to a jejunal DL that was difficult to localize. In this case, the metallic coils used as a radiopaque marker allowed surgeons to accurately identify the bleeding site during intraoperative enteroscopy and successfully manage the lesion with minimally invasive laparoscopic surgery.
Mai, Huynh Nhu,Lee, Sung Hoon,Sharma, Garima,Kim, Dae-Joong,Sharma, Naveen,Shin, Eun-Joo,Pham, Duc Toan,Trinh, Quynh Dieu,Jang, Choon-Gon,Nah, Seung-Yeol,Jeong, Ji Hoon,Kim, Hyoung-Chun Elsevier 2019 Chemico-biological interactions Vol.297 No.-
<P><B>Abstract</B></P> <P>We investigated whether protein kinase Cδ (PKCδ) mediates cocaine-induced hepatotoxicity in mice. Cocaine treatment (60 mg/kg, i.p.) significantly increased cleaved PKCδ expression in the liver of wild-type (WT) mice, and led to significant increases in oxidative parameters (i.e., reactive oxygen species, 4-hydroxylnonenal and protein carbonyl). These cocaine-induced oxidative burdens were attenuated by pharmacological (i.e., rottlerin) or genetic depletion of PKCδ. We also demonstrated that treatment with cocaine resulted in significant increases in nuclear factor erythroid-2-related factor 2 (Nrf-2) nuclear translocation and increased Nrf-2 DNA-binding activity in wild-type (WT) mice. These increases were more pronounced in the rottlerin-treated WT or PKCδ knockout mice than in the saline-treated WT mice. Although cocaine treatment increased Nrf-2 nuclear translocation, DNA binding activity, and γ-glutamyl cysteine ligases (i.e., GCLc and GCLm) mRNA expressions, while it reduced the glutathione level and GSH/GSSG ratio. These decreases were attenuated by PKCδ depletion. Cocaine treatment significantly increased alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in the serum of WT mice signifying the hepatic damage. These increases were also attenuated by PKCδ depletion. In addition, cocaine-induced hepatic degeneration in WT mice was evident 1 d post-cocaine. At that time, cocaine treatment decreased Bcl-2 and Bcl-xL levels, and increased Bax, cytosolic cytochrome c, and cleaved caspase-3 levels. Pharmacological or genetic depletion of PKCδ significantly ameliorated the pro-apoptotic properties and hepatic degeneration. Therefore, our results suggest that inhibition of PKCδ, as well as activation of Nrf-2, is important for protecting against hepatotoxicity induced by cocaine.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Cocaine induces hepatotoxicity via oxidative stress and activation of PKCδ. </LI> <LI> Depletion of PKCδ protects from cocaine-induced hepatotoxicity. </LI> <LI> Depletion of PKCδ exerts antioxidant activity via Nrf2-related glutathione system. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Mai, Huynh Nhu,Sharma, Garima,Sharma, Naveen,Shin, Eun-Joo,Kim, Dae-Joong,Pham, Duc Toan,Trinh, Quynh Dieu,Jang, Choon-Gon,Nah, Seung Yeol,Jeong, Ji Hoon,Kim, Hyoung-Chun Elsevier 2019 Biochimie Vol.158 No.-
<P><B>Abstract</B></P> <P>Cocaine, an addictive drug, is known to induce hepatotoxicity via oxidative damage and proapoptosis. Since p53, a tumor suppressor gene, plays a major role in inducing oxidative stress and apoptosis, we examined the role of p53 inhibition against cocaine-induced hepatotoxicity. Cocaine treatment significantly increased oxidative parameters (i.e., reactive oxygen species, 4-hydroxylnonenal, and protein carbonyl) in the liver of wild type (WT) mice. We found that the pharmacological (i.e. pifithrin-α) and genetic (i.e. p53 knockout) inhibition of p53 significantly attenuates cocaine-induced hepatotoxicity. Cocaine treatment increased alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in the serum of mice, signifying hepatic damage. Consistently, these increases were attenuated by inhibition of p53, implying protection against cocaine-induced hepatic damage. In addition, cocaine treatment significantly increased PKCδ, cleaved PKCδ and p53 levels in the liver of WT mice. These increases were followed by the interaction between p53 and PKCδ, and pro-apoptotic consequences (i.e., cytosolic release of cytochrome <I>c</I>, activation of caspase-3, increase in Bax level and decreases in Bcl-2 and Bcl-xL levels). These changes were attenuated by p53 depletion, reflecting that the critical role of PKCδ in p53-mediated apoptotic potentials. Combined, our results suggest that the inhibition of p53 is important for protection against oxidative burdens, pro-apoptotic events, and hepatic degeneration induced by cocaine.</P> <P><B>Highlight</B></P> <P> <UL> <LI> Cocaine induces hepatotoxicity in mice via oxidative stress and p53 activation. </LI> <LI> Interaction of p53 and PKCδ might be important for p53-mediated toxic potentials. </LI> <LI> p53 knockout or PFT-α attenuates hepatotoxic outcomes induced by cocaine in mice. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Mai, Huynh Nhu,Sharma, Naveen,Jeong, Ji Hoon,Shin, Eun-Joo,Pham, Duc Toan,Trinh, Quynh Dieu,Lee, Yu Jeung,Jang, Choon-Gon,Nah, Seung-Yeol,Bing, Guoying,Kim, Hyoung-Chun Elsevier 2019 Neurochemistry International Vol.124 No.-
<P><B>Abstract</B></P> <P>Previously we demonstrated that p53 mediates dopaminergic neurotoxicity via inducing mitochondrial burdens and proapoptotsis. However, little is known about the role of p53 in the excitotoxicity induced by psychostimulant, such as cocaine. Cocaine-induced kindling (convulsive) behaviors significantly increased p53 expression in the brain. Cocaine-induced p53 expression was more pronounced in hippocampus than in striatum or prefrontal cortex. Genetic depletion of p53 significantly attenuated cocaine-induced convulsive behaviors, followed by c-Fos immunoreactivity, and oxidative burdens in the hippocampus of mice. The antioxidant potentials mediated by genetic depletion of p53 were more pronounced in the mitochondrial-than cytosolic-fraction. Depletion of p53 significantly attenuated the changes in mitochondrial transmembrane potential, intramitochondrial Ca<SUP>2+</SUP> level, and mitochondrial oxidative burdens induced by cocaine. Consistently, depletion of p53 significantly inhibited mitochondrial p53 translocation, and cleaved-PKCδ induced by cocaine. In addition, depletion of p53 protected from cytosolic cytochrome c release, and pro-apoptotic changes induced by cocaine. Importantly, the protective/anticonvulsant potentials by genetic depletion of p53 were comparable to those by pifithrin-μ (PFT), a p53 inhibitor. Our results suggest that depletion of p53 offers anticonvulsive and neuroprotective potentials mainly via attenuating mitochondrial oxidative burdens, mitochondrial dysfunction, and pro-apoptotic signalings against cocaine-induced convulsive neurotoxicity.</P> <P><B>Highlights</B></P> <P> <UL> <LI> P53 inhibition protects against cocaine-induced kindling (convulsive) behaviors. </LI> <LI> Cocaine-induced p53 expression is most pronounced in hippocampus. </LI> <LI> Cocaine-induced oxidative stress is more evident in mitochondria than in cytosol. </LI> <LI> P53 depletion attenuates cocaine-induced mitochondrial dysfunction. </LI> <LI> P53 depletion attenuates cocaine-induced pro-apoptotic phenomena. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
This study describes the preparation and characterization of nanocomposites obtained by melt-mixing of poly (ethylene-co-vinyl acetate) (EVA), polylactic acid (PLA), and TiO₂ nanoparticles (TNPs) via three different methods of direct mixing, one-step, and two-step methods. Vinyltrimethoxysilane was used as a surface modifier for the TNPs. The one-step method showed the best suitability for the preparation of EVA/PLA/TiO₂ nanocomposites. The increase in torque and the adhesion of the TNPs with EVA/PLA matrix in these nanocomposites showed enhanced interfacial interactions between EVA, PLA chains, and TNPs. The tensile strength, Young’s modulus, dynamic storage modulus, and thermooxidative stability of the one-step prepared nanocomposites were higher than those of two other nanocomposites and that of the EVA/PLA blend, reaching maximum values at 2.0 wt% of TNPs.