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Dogan Wilcox posted an update 23 days ago
Finally, we demonstrated that overexpression of miR-199a-3p enhanced proliferation-inhibiting effects of MK2206, an inhibitor of Akt, to ESCC cells, which might be related that MK2206 eliminated the activation of miR-199a-3p to p-Akt. selleck compound These findings discover that miR-199a-3p might participate in the carcinogenesis process of ESCC, which provides a new insight for treatment of ESCC.Ultrasound-mediated nanobubble destruction (UMND), which can utilize the physical energy of ultrasound irradiation to improve the transfer efficiency to target cells is becoming one of the most promising carriers for gene delivery. The purpose of this study was to establish cell-penetrating peptide (CPP)-loaded nanobubbles (CNBs) connected with long intergenic nonprotein coding RNA 00511-small interfering RNA (LINC00511-siRNA) and evaluate its feasibility for improving the chemosensitivity of triple-negative breast cancer in vitro. First, fluorescence imaging confirmed the loading of siLINC00511 on CNBs, and the CNBs-siLINC00511 were characterized by the Zetasizer Nano ZS90 analyzer and transmission electron microscopy. Next, cell counting kit 8 assay was used to detect the inhibitory activity of cisplatin on the proliferation of MDA-MB-231 cells, and the 50% inhibition concentration value before and after transfer was calculated. Finally, the silencing effect of siLINC00511 was evaluated in vitro using an apoptosis assay, transwell assay, real time-PCR and western blotting. UMND combined with CNBs could effectively transfer the siRNA to MDA-MB-231 cells, thus evidently reducing the expression of LINC00511. Furthermore, inhibitory activity of cisplatin on MDA-MB-231 cells was enhanced after downregulation of LINC00511 expression. Downregulation of LINC00511 alters expression of cell cycle-related (CDK 6) and apoptosis-related (Bcl-2 and Bax) proteins in MDA-MB-231 cells. These results suggested that siRNA-CNBs may be an ideal vector for the treatment of tumors, with high efficiency RNA interference under the combined action of UMND. It may provide a new therapeutic method for triple negative breast cancer.Hyperammonemic encephalopathy represents a rare adverse effect of several chemotherapeutic agents, occurring in about 0.7% of patients treated with fluoropyrimidines, and it is independent from dihydropyrimidine dehydrogenase deficiency. Instead, its physiopathology is linked to the inhibition of Krebs cycle by fluoroacetate, leading to decreased ATP production, and to the inhibition of the urea cycle. Oxaliplatin seems to induce hyperammonemic encephalopathy in a similar way, acting on mitochondria. Here, we report the intriguing case of acute hyperammonemic encephalopathy in a 65-year-old patient with preserved liver function, who was treated with oxaliplatin and capecitabine for a metastatic, G1, atypical lung carcinoid. We reviewed the literature and found very few reports of oxaliplatin or capecitabine-induced hyperammonemic encephalopathy. Out of five cases of capecitabine-related hyperammonemic encephalopathy analyzed (four plus our case), median time to hyperammonemic encephalopathy onset was 6 days, with median serum ammonia levels of 213 μmol/L. Oxaliplatin-related hyperammonemic encephalopathy analyzed cases were three (two plus ours), with a median time to hyperammonemic encephalopathy of 11 days and median serum ammonia levels of 167 μmol/L. Identified predisposing factors for chemotherapy-induced hyperammonemia, such as dehydration, liver and renal impairment, infections, and sarcopenia were absent in our case. We hypothesize that the combination of a platinum-derivative and a fluoropyrimidine multiplies the risk of hyperammonemic encephalopathy, even in the absence of predisposing factors nor impaired liver function. We therefore suggest to always consider the risk of hyperammonemia when starting fluoropyrimidines-based chemotherapy, especially combined with platinum-derivatives, and to timely investigate neurologic symptoms monitoring ammonia serum levels.
Wolff-Parkinson-White (WPW) is a congenital defect of the cardiac conduction system (CCS), with proliferation of extra embryologic conduction pathways and rapid conduction of electrical impulses. The estimated neonatal incidence of 0.1% to 0.2% may be misrepresented secondary to missed or misdiagnosis. Undiagnosed WPW can result in sudden cardiac death.
To discuss the pathogenesis, manifestations, diagnosis, management, and lifespan implications of WPW in the prenatal and postnatal periods.
A literature review was conducted using PubMed, CINAHL, and Google Scholar (2013-2019). Search terms included (newborn OR infant), wolff parkinson white, pathogenesis, management, and ventricular preexcitation. After removal of duplicates, 267 references were identified, abstracts reviewed, and 30 publications fully evaluated.
Separation of the heart chambers begins around 7 weeks’ gestation with formation of the annulus fibrosis complete after term. The unknown external environmental influence on the development oation. A paucity of evidenced-based literature exists and future research is crucial to understand the true incidence, physiologic effects, and lifespan implications of WPW on neonates.
Smaller preterm infants often receive extra attention with implementation of additional thermoregulation interventions in the delivery room. Yet, these bundles of interventions have largely remained understudied in larger infants.
The purpose of this study was to evaluate initial (or admission) temperatures of infants born weighing 1500 g or more with diagnoses requiring admission to the neonatal intensive care unit (NICU).
Retrospective medical record review of 388 infants weighing 1500 g or more admitted to the NICU between January 2016 and June 2017.
In total, 42.5% of infants weighing 1500 g or more were admitted hypothermic (<36.5°C), 54.4% with a normothermic temperature, and 2.8% were hyperthermic. Of those infants admitted hypothermic, 30.4% had an admission temperature ranging from 36°C to 36.4°C and 12.1% had an admission temperature of less than 36°C. When compared with infants weighing less than 1500 g, who were born at the same institution and received extra thermal support interventions, there was a statistically significant difference (P < .