Recovering from prolonged cardiac arrest induced by electric shock: A case report.

BACKGROUND: Cardiac arrest (CA) induced by electric shock is a rare occurrence, particularly in cases of prolonged CA. Currently, there is limited literature on similar incidents, and we present a relevant case report. CASE SUMMARY: A 27-year-old Asian male man, experiencing respiratory CA due to electric shock, was successfully restored to sinus rhythm after 50 min of cardiopulmonary resuscitation and 8 electrical defibrillation sessions. In the subsequent stages, the patient received multiple organ function protection measures, leading to a successful recovery and eventual discharge from the hospital. CONCLUSION: Prolonging resuscitation time can enhance the chances of survival for patients, this study provide valuable insights into the management of electric shock-induced CA.

RUNX3 plays an important role in As2O3­induced apoptosis and allows cells to overcome MSC­mediated drug resistance.

The interaction between bone marrow stromal cells and leukemia cells is critical for the persistence and progression of leukemia, and this interaction may account for residual disease. However, the link between leukemia cells and their environment is still poorly understood. In our study, runt­related transcription factor 3 (RUNX3) was identified as a novel target gene affected by As2O3 and involved in mesenchymal stem cell (MSC)­mediated protection of leukemia cells from As2O3­induced apoptosis. We observed induction of RUNX3 expression and the translocation of RUNX3 into the nucleus after As2O3 treatment in leukemia cells. In K562 chronic myeloid leukemia cells, downregulation of endogenous RUNX3 compromised As2O3­induced growth inhibition, cell cycle arrest, and apoptosis. In the presence of MSC, As2O3­induced expression of RUNX3 was reduced significantly and this reduction was modulated by CXCL12/CXCR4 signaling. Furthermore, overexpression of RUNX3 restored, at least in part, the sensitivity of leukemic cells to As2O3. We conclude that RUNX3 plays an important role in As2O3­induced cellular responses and allows cells to overcome MSC­mediated drug resistance. Therefore, RUNX3 is a promising target for therapeutic approaches to overcome MSC­mediated drug resistance.

Improved antitumor activity of epirubicin-loaded CXCR4-targeted polymeric nanoparticles in liver cancers.

A liver-targeted drug delivery system (CX-EPNP) composed of PLGA/TPGS was prepared and characterized. The surface of nanoparticle was conjugated with LFC131 peptide to increase the specific interaction of carrier with CXCR4 overexpressing liver cancers to enhance the Epirubicin (EPI) delivery to tumors. The particles were nanosized with size than 150 nm and portrayed a sustained release kinetics suggesting its suitability for cancer targeting. The in vitro cell uptake results showed that the introduction of LFC131 to the nanoparticles could increase significantly the affinity to human hepatic carcinoma cells (HepG2) with approximately a 3-fold improvement in cellular uptake than non-targeted one. A specific receptor-mediated uptake was observed by confocal laser scanning microscopy. In addition, CX-EPNP showed remarkable cytotoxicity towards HepG2 cells, and could effectively inhibit tumor growth. The more significant EPI accumulation from CX-EPNP in the cancer cells gave rise to the enhanced EPI cytotoxicity and cell apoptosis. The CX-EPNP distributed mostly in the xenograft tumor after intravenous administration to mice and adequately remained in the blood for at least 24h. It seemed that CX-EPNP upon intravenous injection avoided rapid recognition by Kupffer cells and adequately remained in the blood. These findings suggest that CX-EPNP could effectively inhibit the growth of liver tumors in situ and could potentially reduce the systemic side effects. However, extensive investigation is still needed to assess the possible applications of the CX-EPNP in humans.

MicroRNA-26a inhibits proliferation by targeting high mobility group AT-hook 1 in breast cancer.

OBJECTIVES: To investigate the crucial role of miR-26a in breast cancer and to validate whether miR-26a could regulate proliferation of breast cancer cells by targeting high mobility group AT-hook 1 (HMGA1). METHODS: Reverse transcription-polymerase chain reaction (RT-PCR) was used to quantify the expression levels of miR-26a in breast cancer and adjacent non-cancerous breast tissues. MTT, cell migration and invasion assay were carried out to characterize the miR-26a function. Finally, to validate the target gene of miR-26a, luciferase reporter assay was employed, followed by RT-PCR and Western blot confirmation. RESULTS: Compared with normal tissues, a significant down-regulation of miR-26a expression was observed in breast cancer tissues (P=0.002). miR-26a suppresses MDA-MB-231 and Mcf-7 breast cancer cell lines proliferation and motility. The luciferase activity was significantly decreased after co-transfection with psiCHECK-2/HMGA1 3'-UTR and miR-26a mimics in comparison with control cells, and qRT-PCR and Western blotting analysis found that HMGA1 expression at the mRNA and protein levels decreased in the miR-26a mimic-treatment group relative to NC. MTT assay showed that down regulation of HMGA1 by siRNA could significantly enhance the tumor-suppressive effect of miR-26a (P < 0.05). CONCLUSIONS: The results of the present study indicate that miR-26a may be associated with human breast carcinogenesis, which inhibits tumor cell proliferation by targeting HMGA1.

Bone marrow mesenchymal stem cells ameliorate hepatic ischemia/reperfusion injuries via inactivation of the MEK/ERK signaling pathway in rats.

BACKGROUND: Primary graft dysfunction or nonfunction after liver transplantation, which is usually caused by ischemia/reperfusion injury (IRI), is a serious clinical problem. Although bone marrow mesenchymal stem cells (MSCs) have shown great potential in cell therapy for IRI in several organs, the mechanism(s) by which MSCs offer protection is unclear. METHODS: In the present study, we injected MSCs systemically via the tail vein in the rat model of 70% hepatic IRI and measured the biochemical and pathologic alterations to evaluate the therapeutic effect of MSC transplantation. Concurrently, H(2)O(2) was used in vitro to mimic oxidative injury and to induce apoptosis in the human normal liver cell line LO2 to evaluate the protective effects of mesenchymal stem cell conditioned medium (MSC-CM) on LO2 cells. RESULTS: The systemic infusion of MSCs led to a significant prevention of liver enzyme release and an improvement in the histology of the acutely injured liver. In vitro assays demonstrated that MSC-CM promoted hepatocyte proliferation and had a direct inhibitory effect on hepatocyte apoptosis induced by H(2)O(2). In addition, we demonstrated that the prevention of MEK/ERK pathway activation played a pivotal role in the protection. CONCLUSIONS: These data suggest that MSC may represent a potential therapeutic strategy to alleviate hepatic ischemia/reperfusion injuries after liver transplantation via inactivation of the MEK/ERK signaling pathway.