Nanotechnology-mediated anti-inflammatory therapy is emerging as a novel strategy for the treatment of inflammation-induced injury. However, one of the main hurdles for these anti-inflammatory nano-drugs is their potential toxic side effects in vivo. Herein, we uncovered that polydopamine (PDA) nanoparticles with their structure and chemical properties similar to melanin, a natural bio-polymer, displayed a significant anti-inflammation therapeutic effect on acute inflammation-induced injury. PDA with enriched phenol groups functioned as a radical scavenger to eliminate reactive oxygen species (ROS) generated during inflammatory responses. As revealed by in vivo photoacoustic imaging with a H2O2-specific nanoprobe, PDA nanoparticles remarkably reduced intracellular ROS levels in murine macrophages challenged with either H2O2 or lipopolysaccharide (LPS). The anti-inflammatory capacity of PDA nanoparticles was further demonstrated in murine models of both acute peritonitis and acute lung injury (ALI), where diminished ROS generation, reduced proinflammatory cytokines, attenuated neutrophil infiltration, and alleviated lung tissue damage were observed in PDA-treated mice after a single dose of PDA treatment. Our work therefore presents the great promise of PDA nanoparticles as a biocompatible nano-drug for anti-inflammation therapy to treat acute inflammation-induced injury.
Background: Pregnancy is a dynamic state involving multiple adaptations that are necessary in order to ensure a continuous supply of essential metabolites to support the growth and the development of the fetus. Objectives: This review article is aimed to discuss important adaptations in metabolism that take place during non-complicated pregnancy. Materials and Methods: We searched the electronic database PubMed for pre-clinical as well as clinical controlled trials reporting the importance of metabolic adaptations during a non-complicated pregnancy. The preferred language was English and the most recent reports were selected to get an updated review. Results: It was observed clearly in the searched literature that metabolic adaptations are a crucial part of pregnancy, as they provide the mother with sufficient energy stores to meet the demands of pregnancy. These adaptions also help in preparing the mother for lactation and also help in providing proper environment for the proper growth of fetus in the womb. Moreover, multiple biomolecules including glucose, fatty acids, ketone bodies, hormones collectively contribute toward these metabolic adaptations. Conclusions: This review article concludes that metabolic adaptations are crucial for proper fetus development.
Congenital heart defects (CHD) affect approximately 7% of infants, and account for 3% of all infant deaths. CHD is most often caused by the defects associated with ductus arteriosus, which is a vessel that usually closes shortly after birth. The types of CHD include tetralogy of fallot, hypoplastic left heart syndrome, pulmonary atresia, total anomalous pulmonary venous return, transposition of great arteries, tricuspid atresia and truncus arteriosus. There are some risk factors that can increase the chance of a fetus developing CHD such as prematurity, an existing CHD in a first-degree relative, genetic syndromes, infections in utero, maternal drug consumptions and disorders. CHD is diagnosed is through different techniques including pulse oximetry, echocardiograms and physical exams. In this review, we examined the current incidence of CHD, the risk factors associated with CHD, the current methods of diagnosis and surgical options used to repair the defects.
Background:Gastric transposition is a relatively novel method of esophageal replacement. The purpose of this retrospective study was to assess the outcomes of long-gap esophageal atresia (LGEA) treated with esophageal replacement using primary gastric transposition in neonates.Methods:Between March 2008 and May 2015, 14 newborns with LGEA were treated in our hospital. They were all found to have gaps of over 3 cm at the time of the surgery and were diagnosed with LGEA. Primary gastric transposition was performed. They also underwent a gastric drainage procedure by pyloromyotomy. The nasogastric tube was removed if no anastomotic fistula was present and oral feeding was initiated. After initial recovery and discharge, the patients were evaluated with outpatient follow-ups or telephone follow-ups from 1 month after the surgery.Results:The mean age of the neonates at the time of the surgery was 32 hours (range, 4–96 h). The mean birth weight was 2550 g (range, 2100–3500 g). There were 2 deaths in this series of patients due to respiratory failure or withdrawal of treatment by the parents, with a mortality rate of 14.3%. Seven of the neonates developed unilateral or bilateral severe pneumonia. Early anastomotic leak occurred in 3 cases and anastomotic strictures occurred in 4 cases. These 4 neonates were able to eat a fairly normal diet after esophageal balloon dilation. Gastroesophageal reflux occurred in 7 of 12 cases. Feeding multiple small meals and postural support for positioning and feeding were instructed for these 7 cases. Subsequently, the symptoms alleviated and they had no additional surgical therapy. None of the neonates had delayed gastric emptying or gastric retention.Conclusion:Primary gastric transposition may be a rewarding reconstructive option in the treatment of LGEA.
This study aimed to explore the regulatory mechanisms of miR-338-3p and matrix metalloproteinase-2 (MMP-2) in neuroblastoma. Putative target interaction regions of miR-338-3p on MMP-2 were predicted by miRcode and miRbase bioinformatics tools. Relative expression of miRNA-338-3p and MMP-2 in neuroblastoma tissues and GI-LI-N and SK-N-SH cells was determined by reverse transcription polymerase chain reaction experiment. Furthermore, the cell proliferation was determined by Cell Counting Kit-8 assay, the cell apoptosis rate was analyzed by flow cytometry assay, and the cell invasion was evaluated by transwell assay. miR-338-3p expression was downregulated, whereas MMP-2 expression was upregulated in metastasis tissue site compared to that in primary tissue site in total. Furthermore, miR-338-3p overexpression suppressed proliferation, invasion, and epithelial–mesenchymal transition (EMT) of neuroblastoma cells but promoted apoptosis, and the knockdown of MMP-2 triggered similar effects. Furthermore, MMP-2 was directly targeted by miR-338-3p, and overexpression of MMP-2 rescued the inhibitory effects of miR-338-3p on human neuroblastoma cell progression. Collectively, these data demonstrated that miR-338-3p could suppress cell growth, invasion, and EMT pathway and induce apoptosis in neuroblastoma cells by targeting MMP-2. MiR-338-3p sponged MMP-2 to regulate the PI3K/AKT pathway in human neuroblastoma cells.
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