When the traditional LT code is used for encoding and decoding, if there is no encoded packets with degree 1 in the remaining encoded groups, the decoding will stop and the decoding cannot be continued. That will affects the decoding efficiency. For this reason, this paper proposes an improved enhanced decoding method. When BP decoding stops, the remaining coded packets will be decoded using the secondary decoding method, which can improves the success rate of decoding.
Patients with triple negative breast cancer (TNBC) have a poor survival rate following chemotherapy due to drug resistance. Notably, the molecular mechanism of drug resistance remains elusive. Between December 2011 and December 2014, 36 TNBC samples were obtained from Liaocheng People's Hospital. Three gemcitabine-resistant MDA-MB-231 cell lines (MDA-MB-231rGEM1, MDA-MB-231rGEM2 and MDA-MB-231rGEM3) were obtained by exposure of MDA-MB-231 cells to increasing concentrations of gemcitabine for >12 months. Reverse transcription-quantitative polymerase chain reaction was performed to detect the expression levels of specific genes, including microRNA (miR)-620, ATP-binding cassette sub-family B member 1 (ABCB1), ABCC10, cytidine monophosphate kinase, deoxycytidine monophosphate deaminase (DCTD), nucleoside diphosphate kinase 1 (NME1), ribonucleoside-diphosphate reductase large subunit (RRM1) and RRMB2. Western blot analysis was performed to assess the protein expression levels of DCTD. Furthermore, cell proliferation was assessed using a Cell Counting Kit-8 assay and cell apoptosis was detected using an Annexin V/Dead Cell Apoptosis kit. Interactions between miR-620 and DCTD were predicted using TargetScan and detected with the dual luciferase reporter assay. Elevation of miR-620 expression levels were detected in two of the assessed gemcitabine-resistant MDA-MB-231 cell lines compared with MDA-MB-231 cells. Gemcitabine induced significant elevation of miR-620 in MDA-MB-231 cells. An increase of DCTD at mRNA and protein expression levels in MDA-MB-231rGEM1 cells was observed compared with those in MDA-MB-231 cells. Results suggested that DCTD was directly regulated by miR-620. Inhibition of miR-620 and overexpression of DCTD reversed gemcitabine resistance in MDA-MB-231rGEM1 cells via inducing cell apoptosis and cell growth arrest. A negative correlation was identified between miR-620 and DCTD mRNA expression levels in patients with TNBC. The present results demonstrated that overexpression of miR-620 could contribute to the development of gemcitabine resistance in patients with TNBC via the direct downregulation of DCTD.
Herbal drugs have been used for thousands of years in the east and have had a recent resurgence in popularity among consumers in the west. However, most of herbal drug are poorly soluble and have hydrophobic properties and poor distribution, leading to reduced bioavailability and hence decreased treatment efficacy, requiring repeated administration or increased dose. In the past few decades, considerable attention has been focused on the development of self-emulsifying drug delivery system (SEDDS) for herbal drugs. SEDDS is isotropic and thermodynamically stable solutions consisting of oil, surfactant, co-surfactant and drug that can spontaneously form oil-in-water micro/nanoemulsion when mixed with water under gentle stirring. The formulation can be a viable alternative to classical formulations to take advantage of their lipophilic nature and to solve their problems of poor solubility, poor bioavailability, low oral absorption and instability. The mechanism of self-emulsification, solubility studies, construction of phase diagram, optimization and characterization of herbal drugs-loaded SEDDS formulation and in situ absorption evaluation of herbal drugs in rat intestine are presented in our article.
Oral colon-targeted drug delivery has attracted many researchers because of its distinct advantages of increasing the bioavailability of the drug at the target site and reducing the side effects. Polysaccharides that are precisely activated by the physiological environment of the colon hold greater promise for colon targeting. Considerable research efforts have been directed towards developing polysaccharide-based micro/nanocarriers. Types of polysaccharides for colon targeting and in vitro/in vivo assessments of polysaccharide-based carriers for oral colon-targeted drug delivery are summarised. Polysaccharide-based microspheres have gained increased importance not just for the delivery of the drugs for the treatment of local diseases associated with the colon (colon cancer, inflammatory bowel disease (IBD), amoebiasis and irritable bowel syndrome (IBS)), but also for it's potential for the delivery of anti-rheumatoid arthritis and anti-chronic stable angina drugs. Besides, Polysaccharide-based micro/nanocarriers such as microbeads, microcapsules, microparticles, nanoparticles, nanogels and nanospheres are also introduced in this review.
Beidou satellite communication system has the function of short message transmission. The traditional short message "broadcast" function is to use Beidou command aircraft to bind with subordinate end users for "broadcast", which has poor timeliness. This paper designs a short message "broadcast" system using Beidou multi card machine, and carries out data processing at both the sending end and the receiving end, so that it can adapt to various external systems. Through practical verification, when the number of user terminals is not too many, the success rate and timeliness are greatly improved compared with the traditional system.
Abstract Based on the theoretical study on the creative design theory of hybrid bean planting machinery, and combined with the aesthetic characteristics of hybrid bean planting machinery modeling of perceptual engineering-promoted symbiosis mechanism, an innovative design path based on man-machine symbiosis aesthetics of hybrid bean planting machinery was constructed to realize the innovative design style of hybrid bean planting machinery under the background of intelligent age, and thus improving the design level of agricultural machinery finishing.
Background: Chemoresistance greatly hinders the treatment of gastric cancer (GC). Long noncoding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) has been corroborated to be involved in chemoresistance in diverse cancers, including GC. The authors' aim was to investigate the underlying molecular mechanism of PVT1 in cisplatin (DPP) resistance in GC. Methods: Quantitative real-time polymerase chain reaction was conducted to detect the expression levels of PVT1, microRNA (miR)-3619-5p, and transducin beta like 1 x-linked receptor 1 (TBL1XR1) in DDP-resistant GC tissues and cells. 3-(4, 5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry assay were used to check cell viability, half inhibition concentration (IC50), and apoptosis, respectively. The abilities of cell migration and invasion were evaluated by transwell assay. The protein levels of drug resistance-related proteins permeability glycoprotein (P-gp), glutathione s-transferase pi (GST-π), multidrug resistance-associated protein, and TBL1XR1 in samples were measured by Western blot. A xenograft tumor model was established to investigate the biological function of PVT1 in vivo. The starBase site was utilized to predict binding sites between miR-3619-5p and PVT1 or TBL1XR1, and the dual-luciferase reporter assay was performed to verify the interaction. Results: The levels of PVT1 and TBL1XR1 were significantly upregulated in DPP-resistant GC tissues and cells, while miR-3619-5p was notably declined. Knockdown of PVT1 enhanced DPP sensitivity of DPP-resistant GC cells. Also, knockdown of PVT1 enhanced the sensitivity of DPP-resistant GC cells to DPP and inhibited tumor growth in vivo. Meanwhile, PVT1 silencing decreased the expression of drug-resistant proteins. Moreover, PVT1 interacted with miR-3619-5p, and TBL1XR1 was a target of miR-3619-5p. Further studies indicated that downregulation of miR-3619-5p transposed PVT1 silencing- or TBL1XR1 silencing-mediated effects on viability, apoptosis, migration, and invasion of DPP-resistant GC cells. Conclusions: PVT1 silencing attenuated the DPP resistance in GC by downregulating TBL1XR1 via sponging miR-3619-5p.