123 research outputs found
Analysis of Maximum Threshold and Quantum Security for Fault-Tolerant Encoding and Decoding Scheme Base on Steane Code
Steane code is one of the most widely studied quantum error-correction codes,
which is a natural choice for fault-tolerant quantum computation (FTQC).
However, the original Steane code is not fault-tolerant because the CNOT gates
in an encoded block may cause error propagation. In this paper, we first
propose a fault-tolerant encoding and decoding scheme, which analyzes all
possible errors caused by each quantum gate in an error-correction period. In
this scheme, we combine the results of measuring redundant qubits with those of
syndrome measurements to identify specific errors for different types of
errors. But due to the error propagation, there may be cases where different
errors produce the same measurement results. Therefore, we introduce the "flag
qubits" scheme (providing its usage conditions) to reduce error interference as
much as possible, and we consider the errors caused by the introduced quantum
gates, realizing the truly fault-tolerant Steane code. Afterwards, we provide
the fault-tolerant scheme of the universal quantum gate set, including
fault-tolerant preparation and verification of ancillary states. This is the
first time that fault tolerance has been considered for every process of FTQC.
Finally, We propose an algorithm for a more accurate estimation of thresholds
and optimal error-correction period selection. Our simulation results based on
this entire scheme demonstrate the effectiveness of this algorithm, satisfying
the threshold theorem and the currently widely recognized threshold. We analyze
the relationship among the maximum threshold, concatenated levels, and quantum
logical depth, showing that quantum operations play a crucial role in
increasing the threshold. Furthermore, we analyze the computational theoretical
limits of quantum computers from the perspectives of attack and active defense
based on our FTQC scheme, thereby assessing the security of a system
LHPP promotes the intracellular reactive oxygen species accumulation and sensitivity of gastric cancer to cisplatin via JNK and p38 MAPK pathways
Background. Cisplatin is the first-line
chemotherapy drug for the treatment of gastric cancer
(GC) patients. However, GC patients who are resistant to
cisplatin often do not benefit from it. Therefore, finding
a key molecule that affects cisplatin sensitivity is
expected to enhance the efficacy of cisplatin in GC
treatment.
Methods. The human GC cell lines SGC-7901 and
BGC-823 were used. The protein chip array was used to
screen the cisplatin-resistance genes from the complete
response and non-complete response GC patients’
tissues, then, the differential gene expression analysis,
GO function annotation analysis, and KEGG pathway
enrichment analysis were performed. The GC tissue chip
in the GEO database was analyzed to screen the target
gene. Flow cytometry, Hoechst 33342 staining assay,
Western Blot, MTT, tumor sphere formation, cell cycle,
and apoptosis assays were performed to explore the
effect of Phospholysine Phosphohistidine Inorganic
Pyrophosphate Phosphatase (LHPP) on the apoptosis,
stemness, and reactive oxygen species (ROS)
accumulation of cisplatin-resistant GC cells treated with
cisplatin. In vivo, the cisplatin-resistant GC cell lines
transfected with pcDNA-LHPP or si-LHPP were injected
subcutaneously into mice to construct GC subcutaneous
xenograft GC models.
Results. Based on protein chip array and
bioinformatics analysis, it was found that LHPP is the
core molecule in the cisplatin resistance regulatory
network in GC, and its expression is down-regulated in
GC cisplatin-resistant tissues and cells. In vitro and in
vivo experimental results show that the up-regulated
expression of LHPP is closely related to the increase in
sensitivity of GC to cisplatin. Mechanically, we found
that overexpression of LHPP may inhibit the activation
of the JNK and p38 MAPK pathways, promote cisplatininduced ROS accumulation, suppress stemness, and
enhance the sensitivity of GC to cisplatin.
Conclusions. Up-regulation of LHPP may inhibit the
activation of the JNK and p38 MAPK pathways,
attenuate stemness, and enhance the accumulation of
intracellular ROS, thereby promoting cisplatin-mediated
GC cell apoptosis and enhancing cisplatin sensitivity
Tumor Necrosis Factor-α– and Interleukin-1β–Dependent Matrix Metalloproteinase-3 Expression in Nucleus Pulposus Cells Requires Cooperative Signaling via Syndecan 4 and Mitogen-Activated Protein Kinase–NF-κB Axis Implications in Inflammatory Disc Disease
Matrix metalloproteinase-3 (MMP-3) plays an important role in intervertebral disc degeneration, a ubiquitous condition closely linked to low back pain and disability. Elevated expression of syndecan 4, a cell surface heparan sulfate proteoglycan, actively controls disc matrix catabolism. However, the relationship between MMP-3 expression and syndecan 4 in the context of inflammatory disc disease has not been clearly defined. We investigated the mechanisms by which cytokines control MMP-3 expression in rat and human nucleus pulposus cells. Cytokine treatment increased MMP-3 expression and promoter activity. Stable silencing of syndecan 4 blocked cytokine-mediated MMP-3 expression; more important, syndecan 4 did not mediate its effects through NF-κB or mitogen-activated protein kinase (MAPK) pathways. However, treatment with MAPK and NF-κB inhibitors resulted in partial blocking of the inductive effect of cytokines on MMP-3 expression. Loss-of-function studies confirmed that NF-κB, p38α/β2/γ/δ, and extracellular signal–regulated kinase (ERK) 2, but not ERK1, contributed to cytokine-dependent induction of MMP3 promoter activity. Similarly, inhibitor treatments, lentiviral short hairpin-p65, and short hairpin-IκB kinase β significantly decreased cytokine-dependent up-regulation in MMP-3 expression. Finally, we show that transforming growth factor-β can block the up-regulation of MMP-3 induced by tumor necrosis factor (TNF)-α by counteracting the NF-κB pathway and syndecan 4 expression. Taken together, our results suggest that cooperative signaling through syndecan 4 and the TNF receptor 1–MAPK–NF-κB axis is required for TNF-α–dependent expression of MMP-3 in nucleus pulposus cells. Controlling these pathways may slow the progression of intervertebral disc degeneration and matrix catabolism
Biomolecule-assisted synthesis of 3D structure gold nanocrystals in the presence of cystamine dihydrochloride or cysteamine
A facile cystamine-assisted route was designed for the selectively controlled synthesis of 1D and novel, interesting 3D gold litchi-like nanostructures. By controlling reaction conditions such as the molar ratio between HAuCl(4) and cystamine dihydrochloride and the reaction time, the synthesis of various 3D architectural structures and 1D structure in large quantities can be controlled. The formation mechanism for the gold litchi-like assemblies with well-arranged nanorods was also discussed. In addition, as the control test, featheriness gold structures were obtained through using cysteamine as the assisted agent. On the basis of the results from SEM studies and our analysis, we speculate that the different morphologies obtained by cystamine dihydrochloride and cysteamine due to the Au-S interaction. These differences in hydrogen storage capacity are likely due to the size and density of space/pores as well as the morphology of different nanostructures. This facile, environmentally benign, and - solution-phase biomolecule-assisted method can be potentially extended to the preparation of other metal nanostructures
Catestatin Enhances Neuropathic Pain Mediated by P2X4 Receptor of Dorsal Root Ganglia in a Rat Model of Chronic Constriction Injury
Background/Aims: Neuropathic pain (NPP) is the consequence of a number of central nervous system injuries or diseases. Previous studies have shown that NPP is mediated by P2X4 receptors that are expressed on satellite glial cells (SGCs) of dorsal root ganglia (DRG). Catestatin (CST), a neuroendocrine multifunctional peptide, may be involved in the pathogenesis of NPP. Here, we studied the mechanism through which CST affects NPP. Methods: We made rat models of chronic constriction injury (CCI) that simulate neuropathic pain. Rat behavioral changes were estimated by measuring the degree of hyperalgesia as assessed by the mechanical withdrawal threshold (MWT) and the thermal withdrawal latency (TWL). P2X4 mRNA expression was detected by quantitative real-time reverse transcription-polymerase chain reaction. P2X4 protein level and related signal pathways were assessed by western blot. Additionally, double-labeled immunofluorescence was employed to visualize the correspondence between the P2X4 receptor and glial fibrillary acidic protein. An enzyme-linked immunosorbent assay was performed to determine the concentration of CST and inflammatory factors. Results: CST led to lower MWT and TWL and increased P2X4 mRNA and protein expression on the SGCs of model rats. Further, CST upregulated the expression of phosphor-p38 and phosphor-ERK 1/2 on the SGCs of CCI rats. However, the expression level of phosphor-JNK and phosphor-p65 did not obviously change. Conclusion: Taken together, CST might boost NPP by enhancing the sensitivity of P2X4 receptors in the DRG of rats, which would provide us a novel perspective and research direction to explore new therapeutic targets for NPP
pH-responsive stearic acid- O -carboxymethyl chitosan assemblies as carriers delivering small molecular drug for chemotherapy
Abstract(#br)Recently, chemotherapy is still widely exploited to treat the residual, infiltrative tumor cells after surgical resection. However, many anticancer drugs are limited in clinical application due to their poor water-solubility (hydrophibic) and stability, low bioavailability, and unfavorable pharmacokinetics. Herein, an amphiphilic stearic acid- O -carboxymethyl chitosan (SA-CMC) conjugate was synthesized by amide linkage of SA to the backbone of CMC polymer and then self-assembled into nanoparticles (SA-CMC NPs) with the hydrodynamic particle size of ~100 nm. Subsequently, Paclitaxel (PTX) as a potent and broad-spectrum anticancer drug was loaded into SA-CMC NPs by a probe sonication combined with dialysis method. Owing to the multi-hydrophobic inner cores, the prepared PTX-SA-CMC NPs showed a considerable drug-loading capacity of ~19 wt% and a biphasic release behavior with an accumulative release amount in the range of 70–90% within 72 h. PTX-SA-CMC NPs remarkably enhanced the accumulation at the tumor sites by passive targeting followed by cellular endocytosis. Upon the stimuli of acid, PTX-SA-CMC NPs showed exceptional instability by pH change, thereby triggering the rapid disassembly and accelerated drug release. Consequently, compared with Cremophor EL-based free PTX treatment, PTX-SA-CMC NPs under pH-stimuli accomplished highly efficient apoptosis in cancer cells and effectively suppression of tumors by chemotherapy. Overall, PTX-SA-CMC NPs integrating imaging capacity might be a simple yet feasible PTX nanosystem for tumor-targeted delivery and cancer therapy
pH-responsive stearic acid-O-carboxymethyl chitosan assemblies as carriers delivering small molecular drug for chemotherapy.
Recently, chemotherapy is still widely exploited to treat the residual, infiltrative tumor cells after surgical resection. However, many anticancer drugs are limited in clinical application due to their poor water-solubility (hydrophibic) and stability, low bioavailability, and unfavorable pharmacokinetics. Herein, an amphiphilic stearic acid-O-carboxymethyl chitosan (SA-CMC) conjugate was synthesized by amide linkage of SA to the backbone of CMC polymer and then self-assembled into nanoparticles (SA-CMC NPs) with the hydrodynamic particle size of ~100 nm. Subsequently, Paclitaxel (PTX) as a potent and broad-spectrum anticancer drug was loaded into SA-CMC NPs by a probe sonication combined with dialysis method. Owing to the multi-hydrophobic inner cores, the prepared PTX-SA-CMC NPs showed a considerable drug-loading capacity of ~19 wt% and a biphasic release behavior with an accumulative release amount in the range of 70-90% within 72 h. PTX-SA-CMC NPs remarkably enhanced the accumulation at the tumor sites by passive targeting followed by cellular endocytosis. Upon the stimuli of acid, PTX-SA-CMC NPs showed exceptional instability by pH change, thereby triggering the rapid disassembly and accelerated drug release. Consequently, compared with Cremophor EL-based free PTX treatment, PTX-SA-CMC NPs under pH-stimuli accomplished highly efficient apoptosis in cancer cells and effectively suppression of tumors by chemotherapy. Overall, PTX-SA-CMC NPs integrating imaging capacity might be a simple yet feasible PTX nanosystem for tumor-targeted delivery and cancer therapy
Effect of pH on the Interaction of Gold Nanoparticles with DNA and Application in the Detection of Human p53 Gene Mutation
Science and Technology Innovation Project of Fujian Province for Young Scientific Researchers, China [2006F3128]; Open Fund of State Key Laboratory for Physical Chemistry of Solid Surfaces, Xiamen University [200602]Gold nanoparticles (GNPs) are widely used to detect DNA. We studied the effect of pH on the assembly/disassembly of single-stranded DNA functionalized GNPs. Based on the different binding affinities of DNA to GNPs, we present a simple and fast way that uses HCl to drive the assembly of GNPs for detection of DNA sequences with single nucleotide differences. The assembly is reversible and can be switched by changing the solution pH. No covalent modification of DNA or GNP surface is needed. Oligonucleotide derived from human p53 gene with one-base substitution can be distinguished by a color change of the GNPs solution or a significant difference of the maximum absorption wavelength (lambda(max)), compared with wildtype sequences. This method enables detection of 10 picomole quantities of target DNA
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