Experimental Virtual Distillation of Entanglement and Coherence.

Noise is, in general, inevitable and detrimental to practical and useful quantum communication and computation. Under the resource theory framework, resource distillation serves as a generic tool to overcome the effect of noise. Yet, conventional resource distillation protocols generally require operations on multiple copies of resource states, and strong limitations exist that restrict their practical utilities. Recently, by relaxing the setting of resource distillation to only approximating the measurement statistics instead of the quantum state, a resource-frugal protocol, "virtual resource distillation," is proposed, which allows more effective distillation of noisy resources. Here, we report its experimental implementation on a photonic quantum system for the distillation of quantum coherence (up to dimension four) and bipartite entanglement. We show the virtual distillation of the maximal superposed state of dimension four from the state of dimension two, an impossible task in conventional coherence distillation. Furthermore, we demonstrate the virtual distillation of entanglement with operations acting only on a single copy of the noisy Einstein-Podolsky-Rosen (EPR) pair and showcase the quantum teleportation task using the virtually distilled EPR pair with a significantly improved fidelity of the teleported state. These results illustrate the feasibility of the virtual resource distillation method and pave the way for accurate manipulation of quantum resources with noisy quantum hardware.

Effects of amoxicillin and metronidazole as an adjunct to scaling and root planing on glycemic control in patients with periodontitis and type 2 diabetes: A short-term randomized controlled trial.

OBJECTIVE: To assess the effects of amoxicillin and metronidazole with scaling and root planing (SRP) on periodontal parameters and glycemic control in patients with severe periodontitis and diabetes mellitus. BACKGROUND: Adjunctive antibiotics use is advantageous for treating periodontitis in patients with severe periodontitis and diabetes. However, the effects of adjunctive antibiotic use on hemoglobin A1c (HbA1c) levels remain unclear. METHODS: This short-term, randomized controlled trial enrolled patients with severe periodontitis and type 2 diabetes. The patients were randomly allocated to SPR only (i.e., control) or SPR + antibiotics (500 mg of amoxicillin and 200 mg of metronidazole, three times daily for 7 days) groups. Periodontal and hematological parameters were assessed at baseline and 3 months after treatment. Inter- and intra-group analyses were performed using Student's t-tests, Mann-Whitney U tests, and the binary logistic regression models. p-values of <.05 were considered statistically significant. RESULTS: This study enrolled 49 patients, with 23 and 26 patients in the SRP-only and SRP + antibiotics groups, respectively. The periodontal parameters improved significantly and similarly in both groups after treatment (p < .05). The SRP + antibiotics group had more sites of improvement than the SRP-only group when the initial probing depth was >6 mm. (698 [78.96%] vs. 545 [73.35%], p = .008). The HbA1c levels decreased in the SRP-only and SRP + antibiotics groups after treatment (0.39% and 0.53%, respectively). The multivariable binary logistic regression model demonstrated that antibiotics administration and a high baseline HbA1c level were associated with a greater reduction in the HbA1c level (odds ratio = 4.551, 95% confidence interval: 1.012-20.463; odds ratio = 7.162, 95% confidence interval: 1.359-37.753, respectively). CONCLUSIONS: SRP and SRP plus systemic antibiotics were beneficial for glycemic control. Adjunctive antibiotic use slightly improved the outcome for patients with severe periodontitis and poorly controlled diabetes.

Anti-inflammatory effect of Lactiplantibacillus plantarum T1 cell-free supernatants through suppression of oxidative stress and NF-κB- and MAPK-signaling pathways.

Lactiplantibacillus plantarum T1 is an isolated probiotic lactic acid bacterium (LAB) from pickled vegetables in Chongqing, China. In this study, we evaluated the anti-inflammatory activity and the underlying mechanisms of L. plantarum T1 cell-free supernatant (CFS) on lipopolysaccharide (LPS)-stimulated murine RAW264.7 macrophages in vitro. Reverse transcription quantitative PCR (RT-qPCR), immunofluorescence, Griess methods, and western blotting were utilized to assess the anti-inflammatory cytokines and antioxidative effect of L. plantarum T1 CFS. Our results showed that L. plantarum T1 CFS pretreatment significantly reduced pro-inflammatory cytokine levels, including nitric oxide, inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor, interleukin (IL)-1ß, and IL-6, as well as reactive oxygen species. Interestingly, L. plantarum T1 CFS unregulated the antioxidant indicators, including superoxide dismutase, catalase, and glutathione in RAW264.7 cells. Furthermore, L. plantarum T1 CFS activated the nuclear factor kappa-B (NF-κB) and mitogen-activated protein kinase (MAPK) pathway. This study showed the excellent antioxidant and anti-inflammatory properties of L. plantarum T1 through multiple pathways, highlighting its potential for further research and application as a probiotic strain.IMPORTANCEL. plantarum T1 stood out in a series of acid and bile salt tolerance and bacterial inhibition tests as a probiotic isolated from paocai, which provides many health benefits to the host by inhibiting the growth of harmful pathogenic microorganisms and suppressing excessive levels of oxidative stress and inflammation. Not all LAB have good probiotic functions and are used in various applications. The anti-inflammatory antioxidant potential and mechanisms of L. plantarum T1 CFS have not been described and reported. By using RT-qPCR, Griess method, and western blotting, we showed that L. plantarum T1 CFS had anti-inflammatory and antioxidant effects. Griess assay, TBA assay, WST-8 assay, immunofluorescence assay, RT-qPCR, and western blotting data revealed that its anti-inflammatory and antioxidant mechanisms were associated with oxidative stress and NF-κB and MAPK signaling pathways. The anti-inflammatory and antioxidant effects of L. plantarum T1 CFS in paocai generates opportunities for probiotic product development.

Colchicine Attenuates Microvascular Obstruction after Myocardial Ischemia-Reperfusion Injury by Inhibiting the Proliferation of Neutrophil in Bone Marrow.

PURPOSE: Complete and rapid recanalization of blood flow by percutaneous coronary intervention (PCI) is the most effective intervention for patients with ST-segment elevation myocardial infarction (STEMI). However, myocardial ischemia/reperfusion (I/R) injury leads to microvascular obstruction (MVO), limiting its efficacy. Colchicine can reduce myocardial I/R injury, but its effect on MVO is unclear. Hence, this study aimed to assess the role and mechanism of colchicine on MVO. METHODS: Clinical data on STEMI patients with PCI were collected and risk factors related to MVO were analyzed. The rat myocardial I/R model was established to evaluate the MVO by thioflavin S staining. The myocardial I/R model of mice was treated with PBS or colchicine at the reperfusion. The effect of colchicine on cardiomyocyte apoptosis after I/R was evaluated by TUNEL and expression of cleaved caspase-3. ROS levels were detected in H9c2 cells to evaluate the colchicine effect on myocardial oxidative stress. Moreover, the mechanism through which colchicine attenuated MVO was examined using flow cytometry, WB, ELISA, immunohistochemistry, bioinformatics analysis, and immunofluorescence. RESULTS: Multivariate analysis showed that elevated neutrophils were associated with extensive MVO. Colchicine could attenuate MVO and reduce neutrophil recruitment and NETs formation after myocardial I/R. In addition, colchicine inhibited cardiomyocyte apoptosis in vivo and ROS levels in vitro. Furthermore, colchicine inhibited neutrophil proliferation in the bone marrow (BM) by inhibiting the S100A8/A9 inflammatory signaling pathway. CONCLUSIONS: Colchicine attenuated MVO after myocardial I/R injury by inhibiting the proliferation of neutrophils in BM through the neutrophil-derived S100A8/A9 inflammatory signaling pathway.

Reduced Survival and Resistance of Rhodotorula mucilaginosa Following Inhibition of Pigment Production by Naftifine.

Pigments produced by micro-organisms could contribute to their pathogenesis and resistance. The investigation into the red pigment of R. mucilaginosa and its ability to survive and resist has not yet been explored. This study aimed to investigate the survival and resistance of the R. mucilaginosa CQMU1 strain following inhibition of pigment production by naftifine and its underlying mechanism. The red-pigmented Rhodotorula mucilaginosa CQMU1 yeast was isolated from an infected toenail of a patient with onychomycosis. Cultivation of R. mucilaginosa in liquid and solid medium showed the effect of naftifine after treatment. Then, analysis of phagocytosis and tolerance to heat or chemicals of R. mucilaginosa was used to evaluate the survival and resistance of yeast to different treatments. Naftifine reversibly inhibited the pigmentation of R. mucilaginosa CQMU1 in solid and liquid media. Depigmented R. mucilaginosa CQMU1 showed increased susceptibility toward murine macrophage cells RAW264.7 and reduced resistance toward different types of chemicals, such as 1.5-M NaCl and 0.5% Congo red. Inhibition of pigment production by naftifine affected the survival and growth of R. mucilaginosa and its resistance to heat and certain chemicals. The results obtained could further elucidate the target of new mycosis treatment.

An engineered abcb4 expression model reveals the central role of NF-κB in the regulation of drug resistance in zebrafish.

Multi-drug resistance (MDR) is a phenomenon that tumor cells are exposed to a chemotherapeutic drug for a long time and then develop resistance to a variety of other anticancer drugs with different structures and different mechanisms. The in vitro studies of tumor cell lines cannot systematically reflect the role of MDR gene in vivo, and the cost of in vivo studies of transgenic mice as animal models is high. Given the myriad merits of zebrafish relative to other animal models, we aimed to establish a screening system using zebrafish stably expressing ATP-binding cassette (ATP-cassette) superfamily transporters and unveil the potential regulatory mechanism. We first used the Tol2-mediated approach to construct a Tg (abcb4:EGFP) transgenic zebrafish line with ATP-binding cassette (ABC) subfamily B member 4 (abcb4) gene promoter to drive EGFP expression. The expression levels of abcb4 and EGFP were significantly increased when Tg(abcb4:EGFP) transgenic zebrafish embryos were exposed to doxorubicin (DOX) or vincristine (VCR), and the increases were accompanied by a marked decreased accumulation of rhodamine B (RhB) in embryos, indicating a remarkable increase in DOX or VCR efflux. Mechanistically, Akt and Erk signalings were activated upon the treatment with DOX or VCR. With the application of Akt and Erk inhibitors, drug resistance was reversed with differing responsive effects. Notably, downstream NF-κB played a central role in the regulation of abcb4-mediated drug resistance. Taken together, the data indicate that the engineered Tg(abcb4:EGFP) transgenic zebrafish model is a new platform for screening drug resistance in vivo, which may facilitate and accelerate the process of drug development.

Experimental Quantum State Measurement with Classical Shadows.

A crucial subroutine for various quantum computing and communication algorithms is to efficiently extract different classical properties of quantum states. In a notable recent theoretical work by Huang, Kueng, and Preskill [Nat. Phys. 16, 1050 (2020)NPAHAX1745-247310.1038/s41567-020-0932-7], a thrifty scheme showed how to project the quantum state into classical shadows and simultaneously predict M different functions of a state with only O(log_{2}M) measurements, independent of the system size and saturating the information-theoretical limit. Here, we experimentally explore the feasibility of the scheme in the realistic scenario with a finite number of measurements and noisy operations. We prepare a four-qubit GHZ state and show how to estimate expectation values of multiple observables and Hamiltonians. We compare the measurement strategies with uniform, biased, and derandomized classical shadows to conventional ones that sequentially measure each state function exploiting either importance sampling or observable grouping. We next demonstrate the estimation of nonlinear functions using classical shadows and analyze the entanglement of the prepared quantum state. Our experiment verifies the efficacy of exploiting (derandomized) classical shadows and sheds light on efficient quantum computing with noisy intermediate-scale quantum hardware.

Serum exosomal microRNA transcriptome profiling in subacute spinal cord injured rats.

MicroRNAs (miRNAs) are involved in a series of pathology of spinal cord injury (SCI). Although, locally expressed miRNAs have advantages in studying the pathological mechanism, they cannot be used as biomarkers. The "free circulation" miRNAs can be used as biomarkers, but they have low concentration and poor stability in body fluids. Exosomal miRNAs in body fluids have many advantages comparing with free miRNAs. Therefore, we hypothesized that the specific miRNAs in the central nervous system might be transported to the peripheral circulation and concentrated in exosomes after injury. Using next-generation sequencing, miRNA profiles in serum exosomes of sham and subactue SCI rats were analyzed. The results showed that SCI can lead to changes of serum exosomal miRNAs. These changed miRNAs and their associated signaling pathways may explain the pathological mechanism of suacute SCI. More importantly, we found some valuable serum exosomal miRNAs for diagnosis and prognosis of SCI.

Serum exosomal microRNA transcriptome profiling in subacute spinal cord injured rats.

MicroRNAs (miRNAs) are involved in a series of pathology of spinal cord injury (SCI). Although, locally expressed miRNAs have advantages in studying the pathological mechanism, they cannot be used as biomarkers. The "free circulation" miRNAs can be used as biomarkers, but they have low concentration and poor stability in body fluids. Exosomal miRNAs in body fluids have many advantages comparing with free miRNAs. Therefore, we hypothesized that the specific miRNAs in the central nervous system might be transported to the peripheral circulation and concentrated in exosomes after injury. Using next-generation sequencing, miRNA profiles in serum exosomes of sham and subactue SCI rats were analyzed. The results showed that SCI can lead to changes of serum exosomal miRNAs. These changed miRNAs and their associated signaling pathways may explain the pathological mechanism of suacute SCI. More importantly, we found some valuable serum exosomal miRNAs for diagnosis and prognosis of SCI.

The Tightness of Multipartite Coherence from Spectrum Estimation.

Detecting multipartite quantum coherence usually requires quantum state reconstruction, which is quite inefficient for large-scale quantum systems. Along this line of research, several efficient procedures have been proposed to detect multipartite quantum coherence without quantum state reconstruction, among which the spectrum-estimation-based method is suitable for various coherence measures. Here, we first generalize the spectrum-estimation-based method for the geometric measure of coherence. Then, we investigate the tightness of the estimated lower bound of various coherence measures, including the geometric measure of coherence, the l1-norm of coherence, the robustness of coherence, and some convex roof quantifiers of coherence multiqubit GHZ states and linear cluster states. Finally, we demonstrate the spectrum-estimation-based method as well as the other two efficient methods. We observe that the spectrum-estimation-based method outperforms other methods in various coherence measures, which significantly enhances the accuracy of estimation.

CRID3, a blocker of apoptosis associated speck like protein containing a card, ameliorates murine spinal cord injury by improving local immune microenvironment.

BACKGROUND: After spinal cord injury (SCI), destructive immune cell subsets are dominant in the local microenvironment, which are the important mechanism of injury. Studies have shown that inflammasomes play an important role in the inflammation following SCI, and apoptosis-associated speck-like protein containing a card (ASC) is the adaptor protein shared by inflammasomes. Therefore, we speculated that inhibiting ASC may improve the local microenvironment of injured spinal cord. Here, CRID3, a blocker of ASC oligomerization, was used to study its effect on the local microenvironment and the possible role in neuroprotection following SCI. METHODS: Murine SCI model was created using an Infinite Horizon impactor at T9 vertebral level with a force of 50 kdynes and CRID3 (50 mg/kg) was intraperitoneally injected following injury. ASC and its downstream molecules in inflammasome signaling pathway were measured by western blot. The immune cell subsets were detected by immunohistofluorescence (IHF) and flow cytometry (FCM). The spinal cord fibrosis area, neuron survival, myelin preservation, and functional recovery were assessed. RESULTS: Following SCI, CRID3 administration inhibited inflammasome-related ASC and caspase-1, IL-1ß, and IL-18 activation, which consequently suppressed M1 microglia, Th1 and Th1Th17 differentiation, and increased M2 microglia and Th2 differentiation. Accordingly, the improved histology and behavior have also been found. CONCLUSIONS: CRID3 may ameliorate murine SCI by inhibiting inflammasome activation, reducing proinflammatory factor production, restoring immune cell subset balance, and improving local immune microenvironment, and early administration may be a promising therapeutic strategy for SCI.

Counting Classical Nodes in Quantum Networks.

Quantum networks illustrate the use of connected nodes of quantum systems as the backbone of distributed quantum information processing. When the network nodes are entangled in graph states, such a quantum platform is indispensable to almost all the existing distributed quantum tasks. Unfortunately, real networks unavoidably suffer from noise and technical restrictions, making nodes transit from quantum to classical at worst. Here, we introduce a figure of merit in terms of the number of classical nodes for quantum networks in arbitrary graph states. Such a network property is revealed by exploiting a novel Einstein-Podolsky-Rosen steerability. Experimentally, we demonstrate photonic quantum networks of n_{q} quantum nodes and n_{c} classical nodes with n_{q} up to 6 and n_{c} up to 18 using spontaneous parametric down-conversion entanglement sources. We show that the proposed method is faithful in quantifying the classical defects in prepared multiphoton quantum networks. Our results provide novel identification of generic quantum networks and nonclassical correlations in graph states.

miR-29c regulates resistance to paclitaxel in nasopharyngeal cancer by targeting ITGB1.

Paclitaxel (Taxol) is an anticancer taxane drug commonly used in the treatment of nasopharyngeal carcinoma (NPC). However, resistance to paclitaxel is a major difficulty in developing an effective therapy against NPC. MicroRNAs (miRNAs) are known to regulate genes that are involved in drug resistance. We assessed the effects of miR-29c, an miRNA identified in a genome-wide study of Taxol resistance, on genes associated with resistance in NPC cells. We established Taxol resistance in two human NPC cell lines, SUNE-1 and C666-1 (SUNE-1-Taxol and C666-1-Taxol) and found that miR-29c was downregulated and integrin beta-1 (ITGB1) was upregulated in Taxol-resistant NPC cells compared with parental NPC cells. Further investigations using a TUNEL assay and BAX/BCL-2 ratio, found that overexpression of miR-29c and knockdown of ITGB1 can resensitize drug-resistant NPC cells to Taxol and promote apoptosis. In addition, a dual-luciferase reporter assay indicated that ITGB1 is the target of miR-29c. Furthermore, silencing miR-29c markedly increased Taxol-resistant NPC tumor growth in a nude mouse xenograft model while knockdown of ITGB1 reversed this result. Overall, these data demonstrate that miR-29c regulates resistance to Taxol in NPC by targeting ITGB1. Our research indicates that miR-29c may have potential use in Taxol-resistant NPC therapy.

Transcriptome profile of rat genes in bone marrow-derived macrophages at different activation statuses by RNA-sequencing.

The underlying mechanisms of macrophage polarization have been detected by genome-wide transcriptome analysis in a variety of mammals. However, the transcriptome profile of rat genes in bone marrow-derived macrophages (BMM) at different activation statuses has not been reported. Therefore, we performed RNA-Sequencing to identify gene expression signatures of rat BMM polarized in vitro with different stimuli. The differentially expressed genes (DEGs) among unactivated (M0), classically activated pro-inflammatory (M1), and alternatively activated anti-inflammatory macrophages (M2) were analyzed by using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis. In this study, not only we have identified the changes of global gene expression in rat M0, M1 and M2, but we have also made clear systematically the key genes and signaling pathways in the differentiation process of M0 to M1 and M2. These will provide a foundation for future researches of macrophage polarization.

Screening antiproliferative drug for breast cancer from bisbenzylisoquinoline alkaloid tetrandrine and fangchinoline derivatives by targeting BLM helicase.

BACKGROUND: The high expression of BLM (Bloom syndrome) helicase in tumors involves its strong association with cell expansion. Bisbenzylisoquinoline alkaloids own an antitumor property and have developed as candidates for anticancer drugs. This paper aimed to screen potential antiproliferative small molecules from 12 small molecules (the derivatives of bisbenzylisoquinoline alkaloids tetrandrine and fangchinoline) by targeting BLM642-1290 helicase. Then we explore the inhibitory mechanism of those small molecules on proliferation of MDA-MB-435 breast cancer cells. METHODS: Fluorescence polarization technique was used to screen small molecules which inhibited the DNA binding and unwinding of BLM642-1290 helicase. The effects of positive small molecules on the ATPase and conformation of BLM642-1290 helicase were studied by the malachite green-phosphate ammonium molybdate colorimetry and ultraviolet spectral scanning, respectively. The effects of positive small molecules on growth of MDA-MB-435 cells were studied by MTT method, colony formation and cell counting method. The mRNA and protein levels of BLM helicase in the MDA-MB-435 cells after positive small molecule treatments were examined by RT-PCR and ELISA, respectively. RESULTS: The compound HJNO (a tetrandrine derivative) was screened out which inhibited the DNA binding, unwinding and ATPase of BLM642-1290 helicase. That HJNO could bind BLM642-1290helicase to change its conformationcontribute to inhibiting the DNA binding, ATPase and DNA unwinding of BLM642-1290 helicase. In addition, HJNO showed its inhibiting the growth of MDA-MB-435 cells. The values of IC50 after drug treatments for 24 h, 48 h and 72 h were 19.9 µmol/L, 4.1 µmol/L and 10.9 µmol/L, respectively. The mRNA and protein levels of BLM helicase in MDA-MB-435 cells increased after HJNO treatment. Those showed a significant difference (P < 0.05) compared with negative control when the concentrations of HJNO were 5 µmol/L and 10 µmol/L, which might contribute to HJNO inhibiting the DNA binding, ATPase and DNA unwinding of BLM helicase. CONCLUSION: The small molecule HJNO was screened out by targeting BLM642-1290 helicase. And it showed an inhibition on MDA-MB-435 breast cancer cells expansion.

MicroRNA-29c Increases the Chemosensitivity of Pancreatic Cancer Cells by Inhibiting USP22 Mediated Autophagy.

BACKGROUND/AIMS: Pancreatic cancer (PC) is an aggressive malignancy with a poor survival rate. Despite advances in the treatment of PC, the efficacy of therapy is limited by the development of chemoresistance. Here, we examined the role of microRNA-29c (miR-29c) and the involvement of autophagy and apoptosis in the chemoresistance of PC cells in vivo and in vitro. METHODS: We employed qRT-PCR, western blot and immunofluorescence to examine the expression level of miR-29c, USP22 and autophagy relative protein. In addition, we used MTT assay to detect cell proliferation and transwell assay to measure migration and invasiveness. The apoptosis was determined using annexin V-FITC/PI apoptosis detection kit by flow cytometry. Luciferase reporter assays confirmed the relationship between USP22 and miR-29c. RESULTS: miR-29c overexpression in the PC cell line PANC-1 enhanced the effect of gemcitabine on decreasing cell viability and inducing apoptosis and inhibited autophagy, as shown by western blotting, immunofluorescence staining, colony formation assays, and flow cytometry. Ubiquitin specific peptidase (USP)-22, a deubiquitinating enzyme known to induce autophagy and promote PC cell survival, was identified as a direct target of miR-29c. USP22 knockdown experiments indicated that USP22 suppresses gemcitabine-induced apoptosis by promoting autophagy, thereby increasing the chemoresistance of PC cells. Luciferase reporter assays confirmed that USP22 is a direct target of miR-29c. A xenograft mouse model demonstrated that miR-29c increases the chemosensitivity of PC in vivo by downregulating USP22, leading to the inhibition of autophagy and induction of apoptosis. CONCLUSIONS: Taken together, these findings reveal a potential mechanism underlying the chemoresistance of PC cells mediated by the regulation of USP22-mediated autophagy by miR-29c, suggesting potential targets and therapeutic strategies in PC.

Increased ceruloplasmin expression caused by infiltrated leukocytes, activated microglia, and astrocytes in injured female rat spinal cords.

Ceruloplasmin (Cp), an enzyme containing six copper atoms, has important roles in iron homeostasis and antioxidant defense. After spinal cord injury (SCI), the cellular components in the local microenvironment are very complex and include functional changes of resident cells and the infiltration of leukocytes. It has been confirmed that Cp is elevated primarily in astrocytes and to a lesser extent in macrophages following SCI in mice. However, its expression in other cell types is still not very clear. In this manuscript, we provide a sensible extension of these findings by examining this system within a female Sprague-Dawley rat model and expanding the scope of inquiry to include additional cell types. Quantitative reverse transcription polymerase chain reaction and Western blot analysis revealed that the Cp mRNA and protein in SCI tissue homogenates were quite consistent with prior publications. However, we observed that Cp was expressed not only in GFAP+ astrocytes (consistent with prior reports) but also in CD11b+ microglia, CNPase+ oligodendrocytes, NeuN+ neurons, CD45+ leukocytes, and CD68+ activated microglia/macrophages. Quantitative analysis proved that infiltrated leukocytes, activated microglia/macrophages, and astrocytes should be the major sources of increased Cp.

Quantum teleportation and entanglement distribution over 100-kilometre free-space channels.

Transferring an unknown quantum state over arbitrary distances is essential for large-scale quantum communication and distributed quantum networks. It can be achieved with the help of long-distance quantum teleportation and entanglement distribution. The latter is also important for fundamental tests of the laws of quantum mechanics. Although quantum teleportation and entanglement distribution over moderate distances have been realized using optical fibre links, the huge photon loss and decoherence in fibres necessitate the use of quantum repeaters for larger distances. However, the practical realization of quantum repeaters remains experimentally challenging. Free-space channels, first used for quantum key distribution, offer a more promising approach because photon loss and decoherence are almost negligible in the atmosphere. Furthermore, by using satellites, ultra-long-distance quantum communication and tests of quantum foundations could be achieved on a global scale. Previous experiments have achieved free-space distribution of entangled photon pairs over distances of 600 metres (ref. 14) and 13 kilometres (ref. 15), and transfer of triggered single photons over a 144-kilometre one-link free-space channel. Most recently, following a modified scheme, free-space quantum teleportation over 16 kilometres was demonstrated with a single pair of entangled photons. Here we report quantum teleportation of independent qubits over a 97-kilometre one-link free-space channel with multi-photon entanglement. An average fidelity of 80.4 ± 0.9 per cent is achieved for six distinct states. Furthermore, we demonstrate entanglement distribution over a two-link channel, in which the entangled photons are separated by 101.8 kilometres. Violation of the Clauser-Horne-Shimony-Holt inequality is observed without the locality loophole. Besides being of fundamental interest, our results represent an important step towards a global quantum network. Moreover, the high-frequency and high-accuracy acquiring, pointing and tracking technique developed in our experiment can be directly used for future satellite-based quantum communication and large-scale tests of quantum foundations.

Targeting Cancer Stem Cells to Overcome Chemoresistance.

Cancers are heterogeneous at the cell level, and the mechanisms leading to cancer heterogeneity could be clonal evolution or cancer stem cells. Cancer stem cells are resistant to most anti-cancer treatments and could be preferential targets to reverse this resistance, either targeting stemness pathways or cancer stem cell surface markers. Gold nanoparticles have emerged as innovative tools, particularly for photo-thermal therapy since they can be excited by laser to induce hyperthermia. Gold nanoparticles can be functionalized with antibodies to specifically target cancer stem cells. Preclinical studies using photo-thermal therapy have demonstrated the feasibility of targeting chemo-resistant cancer cells to reverse clinical chemoresistance. Here, we review the data linking cancer stem cells and chemoresistance and discuss the way to target them to reverse resistance. We particularly focus on the use of functionalized gold nanoparticles in the treatment of chemo-resistant metastatic cancers.

Transcriptome profile of rat genes in injured spinal cord at different stages by RNA-sequencing.

BACKGROUND: Spinal cord injury (SCI) results in fatal damage and currently has no effective treatment. The pathological mechanisms of SCI remain unclear. In this study, genome-wide transcriptional profiling of spinal cord samples from injured rats at different time points after SCI was performed by RNA-Sequencing (RNA-Seq). The transcriptomes were systematically characterized to identify the critical genes and pathways that are involved in SCI pathology. RESULTS: RNA-Seq results were obtained from total RNA harvested from the spinal cords of sham control rats and rats in the acute, subacute, and chronic phases of SCI (1 day, 6 days and 28 days after injury, respectively; n = 3 in every group). Compared with the sham-control group, the number of differentially expressed genes was 1797 in the acute phase (1223 upregulated and 574 downregulated), 6590 in the subacute phase (3460 upregulated and 3130 downregulated), and 3499 in the chronic phase (1866 upregulated and 1633 downregulated), with an adjusted P-value <0.05 by DESeq. Gene ontology (GO) enrichment analysis showed that differentially expressed genes were most enriched in immune response, MHC protein complex, antigen processing and presentation, translation-related genes, structural constituent of ribosome, ion gated channel activity, small GTPase mediated signal transduction and cytokine and/or chemokine activity. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that the most enriched pathways included ribosome, antigen processing and presentation, retrograde endocannabinoid signaling, axon guidance, dopaminergic synapses, glutamatergic synapses, GABAergic synapses, TNF, HIF-1, Toll-like receptor, NF-kappa B, NOD-like receptor, cAMP, calcium, oxytocin, Rap1, B cell receptor and chemokine signaling pathway. CONCLUSIONS: This study has not only characterized changes in global gene expression through various stages of SCI progression in rats, but has also systematically identified the critical genes and signaling pathways in SCI pathology. These results will expand our understanding of the complex molecular mechanisms involved in SCI and provide a foundation for future studies of spinal cord tissue damage and repair. The sequence data from this study have been deposited into Sequence Read Archive ( http://www.ncbi.nlm.nih.gov/sra ; accession number PRJNA318311).