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To reduce the risk of leaking confidential information in nuclear arms control, we propose a new arms control inspection concept based on neutron activation analysis, in conjunction with physical shielding technology to distort the energy and propagation path of the outgoing particles in the physical domain. The reliability and security of this authentication concept are demonstrated using Monte Carlo simulations. It turns out that the concept can readily identify isotope cheats and two typical geometric cheats without revealing sensitive information about the inspected items.

Periodontal tissue is a highly dynamic and frequently stimulated area where homeostasis is easily destroyed, leading to proinflammatory periodontal diseases. Bacteria–bacteria and cell–bacteria interactions play pivotal roles in periodontal homeostasis and disease progression. Several reviews have comprehensively summarized the roles of bacteria and stem cells in periodontal homeostasis. However, they did not describe the roles of extracellular vesicles (EVs) from bacteria and cells. As communication mediators evolutionarily conserved from bacteria to eukaryotic cells, EVs secreted by bacteria or cells can mediate interactions between bacteria and their hosts, thereby offering great promise for the maintenance of periodontal homeostasis. This review offers an overview of EV biogenesis, the effects of EVs on periodontal homeostasis, and recent advances in EV-based periodontal regenerative strategies. Specifically, we document the pathogenic roles of bacteria-derived EVs (BEVs) in periodontal dyshomeostasis, focusing on plaque biofilm formation, immune evasion, inflammatory pathway activation and tissue destruction. Moreover, we summarize recent advancements in cell-derived EVs (CEVs) in periodontal homeostasis, emphasizing the multifunctional biological effects of CEVs on periodontal tissue regeneration. Finally, we discuss future challenges and practical perspectives for the clinical translation of EV-based therapies for periodontitis. Graphical Abstract

Background High glucose-induced damage to the osteogenic differentiation of human periodontal ligament stem cells (PDLSCs) has long been a challenge to periodontal regeneration for diabetic individuals. Metformin is an anti-hyperglycemic drug that exhibits abundant biological activities associated with cell metabolism and downstream tissue regeneration. However, how metformin combats damage to PDLSC osteogenic differentiation under high glucose and the underlying mechanisms remain unknown. Methods Osteogenic differentiation of PDLSCs was assessed by alkaline phosphatase (ALP) staining, ALP activity, Alizarin Red staining and quantitative assay, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot analysis. RNA-seq analysis was performed to screen target genes of metformin, and the effects of target genes were confirmed using lentivirus transfection. Western blot analysis was also used to detect the protein level of underlying signaling pathways. Results We found that osteogenic differentiation of PDLSCs under high glucose was decreased, and metformin addition enhanced this capacity of differentiation. Furthermore, the results of RNA-seq analysis showed that natriuretic peptide receptor 3 (NPR3) was upregulated in PDLSCs under high glucose and downregulated after metformin addition. When the underlying pathways involved were investigated, we found that upregulation of NPR3 can compromise the metformin-enhanced PDLSC osteogenic differentiation and activate the MAPK pathway (especially the p38 MAPK and Erk1/2 pathway), and that inhibition of the NPR3-mediated p38 MAPK or Erk1/2 pathway enhanced the osteogenic differentiation of PDLSCs under high glucose. Conclusions The present study suggests that metformin may enhance the osteogenic differentiation of PDLSCs under high glucose via downregulation of NPR3 and inhibition of its downstream MAPK pathway. This is the first report identifying the involvement of NPR3-mediated MAPK pathway in the metformin-enhanced osteogenic differentiation, indicating that NPR3 antagonists, such as metformin, may be feasible therapeutics for periodontal tissue regeneration in diabetic individuals.

Background High glucose-induced damage to the osteogenic differentiation of human periodontal ligament stem cells (PDLSCs) has long been a challenge to periodontal regeneration for diabetic individuals. Metformin is an anti-hyperglycemic drug that exhibiting abundant biological activities associated with cell metabolism and downstream tissue regeneration. However, how metformin combats damage to PDLSC osteogenic potential under high glucose and the underlying mechanisms remain unknown. Methods Osteogenic differentiation of PDLSCs was assessed by Alkaline phosphatase (ALP) staining, ALP activity, Alizarin red staining and quantitative assay, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot analysis. RNA-seq analysis was performed to screen target genes of metformin, and the effects of target genes were confirmed using lentivirus transfection. Western blot analysis was also used to detect the protein level of underlying signaling pathways. Results Osteogenic differentiation of PDLSCs under high glucose was decreased and metformin addition enhanced the capacity of differentiation. Furthermore, natriuretic peptide receptor 3 (NPR3) was upregulated in PDLSCs under high glucose and downregulated after metformin addition. Additionally, we demonstrated that upregulation of NPR3 compromised the metformin-enhanced PDLSC osteogenic differentiation through activating the MAPK pathway, and that inhibition of p38 MAPK or Erk1/2 pathway enhanced the osteogenic differentiation of PDLSCs with NPR3 upregulation. Conclusions The present study suggests that metformin may enhance the osteogenic differentiation of PDLSCs under high glucose via downregulation of NPR3 and inhibition of its downstream MAPK pathway. This is the first report identifying the involvement of NPR3-mediated MAPK pathway in the metformin-enhanced osteogenic differentiation, indicating that NPR3 antagonists, such as metformin, may be feasible therapeutics for periodontal tissue regeneration in diabetic individuals.

Recently, strategies that can target the underlying mechanisms of phenotype change to modulate the macrophage immune response from the standpoint of biological science have attracted increasing attention in the field of biomaterials. In this study, we printed a molybdenum-containing bioactive glass ceramic (Mo-BGC) scaffold as an immunomodulatory material. In a clinically relevant critical-size periodontal defect model, the defect-matched scaffold featured robust immunomodulatory activity, enabling long-term stable macrophage modulation and leading to enhanced regeneration of multiple periodontal tissues in canines. Further studies demonstrated that the regeneration-enhancing function of Mo-BGC scaffold was macrophage-dependent by using canines with host macrophage depletion. To investigate the role of Mo in material immunomodulation, in vitro investigations were performed and revealed that Mo-BGC powder extract, similar to MoO

The predictive power of the deformed relativistic Hartree-Bogoliubov theory in continuum (DRHBc) for nuclear mass is examined in the superheavy region, $102 \le Z \le 120$. The accuracy of predicting the 10 (56) measured (measured and empirical) masses is $0.635$ ($0.642$) MeV, in comparison with $0.515$ ($1.360$) MeV by WS4 and $0.910$ ($2.831$) MeV by FRDM. Possible stability against multineutron emission beyond the two-neutron drip line is explored by the DRHBc theory, which takes into account simultaneously the deformation effects, the pairing correlations, and the continuum effects. Nuclei stable against two- and multineutron emissions beyond the two-neutron drip line are predicted in $_{106}$Sg, $_{108}$Hs, $_{110}$Ds, and $_{112}$Cn isotopic chains, forming a peninsula of stability adjacent to the nuclear mainland. This stability is mainly due to the deformation which significantly affects the shell structure around the Fermi surface. The pairing correlations and continuum influence the stability peninsula in a self-consistent way., 13 pages, 5 figures, minor updates according to the published version

Although substantial data indicate that the osteogenic potential of periodontal ligament stem cells (PDLSCs) is compromised under inflammatory conditions, the underlying mechanism remains largely unexplored. In this study, we found that both the autophagy levels and autophagic flux levels were decreased in PDLSCs incubated under inflammatory conditions (I-PDLSCs). Based on the increased expression of LC3 II (at an autophagy level) and decreased accumulation of LC3 II (at an autophagic flux level) in I-PDLSCs, we speculated that the disruption of I-PDLSC autophagy arose from dysfunction of the cellular autophagy-lysosome system. Subsequently, our hypothesis was demonstrated by inhibited autophagosome-lysosome fusion, damaged lysosomal function, and suppressed activation of transcription factor EB (TFEB, a master regulator of the autophagy-lysosome system) in I-PDLSCs and verified by TFEB overexpression in I-PDLSCs. We found that gold nanoparticle (Au NP) treatment rescued the osteogenic potential of I-PDLSCs by restoring the inflammation-compromised autophagy-lysosome system. In this context, Au NP ceased to be effective when TFEB was knocked down in PDLSCs. Our data demonstrate the crucial role of the autophagy-lysosome system in cellular osteogenesis under inflammatory conditions and suggest a new target for rescuing inflammation-induced cell dysfunction using nanomaterials to aid cell biology and tissue regeneration.

Bone cancer pain (BCP) profoundly compromises the life quality of patients with bone metastases. Severe side effects of the drugs which were widely used and effective in the various stages of this condition results in a huge challenge for BCP treatment. Here, we investigated the antinociceptive effects of XPro1595, a soluble tumor necrosis factor (solTNF) inhibitor with considerable immunoregulatory efficacy, on BCP, as well as the underlying mechanisms within the spinal dorsal horn (SDH). Walker 256 mammary gland carcinoma cells were intratibially inoculated to induce BCP. Intrathecal administration of XPro1595 alleviated bone cancer-induced chronic pain in a dose-dependent manner, with an ED50 of 9.69 mg/kg. Bone cancer resulted in the activation of astrocytes and microglia in the SDH through the upregulation of mitogen-activated protein kinase (MAPK) pathways, which was accompanied by an over-expression of pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6. XPro1595suppressed bone cancer-evoked glial activation and the consequent neuroinflammation. These inhibitory effects of XPro1595 were, at least partially, mediated by a reduction in the phosphorylation of p38 MAPK in spinal glial cells. In conclusion, inhibition of spinal glia by XPro1595 may have utility in the treatment of bone cancer-induced neuroinflammation, and our results further implicate XPro1595 as a new promising therapeutic agent for BCP.

Recently, we found that although high-stiffness matrices stimulated osteogenic differentiation of bone marrow-derived stromal cells (BMSCs), the macrophages (Mφs) in high-stiffness transglutaminase crosslinked gelatins (TG-gels) tended to undergo M1 polarization and hence compromised cell osteogenesis. In this study, we hypothesized that the copresentation of interleukin (IL)-4 and stromal cell-derived factor (SDF)-1α in high-stiffness TG-gels may enhance periodontal regeneration by modulating Mφ polarization and promoting endogenous stem cell recruitment. We found that Mφs were more likely to polarize toward an immunomodulatory M2 state in the presence of IL-4 and hence positively influence the osteogenic differentiation of BMSCs when these cells coexisted in either indirect or direct co-culture systems. In cell migration assays, BMSCs exhibited an enhanced capability to move toward gels containing SDF-1α, and more cells could be recruited into the three-dimensional matrix of TG-gels. When TG-gels containing IL-4 and/or SDF-1α were used to repair periodontal defects, more new bone (MicroCT) was formed in animals that received the dual cytokine-loaded transplants at 4 weeks postsurgery. Mφs were recruited to all the transplanted gels, and after one week, more M1-phenotype cells were found in the groups without IL-4, while the presence of IL-4 was more likely to result in M2 polarization (immunofluorescence staining). When the tissue biopsies were histologically examined, the TG-gels containing both IL-4 and SDF-1α led to a generally satisfactory regeneration with respect to attachment recovery (epithelial and connective tissue) and hybrid tissue regeneration (bone, periodontal ligament and cementum). Our data suggest that the incorporation of IL-4 into high-stiffness TG-gels may promote the M2 polarization of Mφs and that SDF-1α can be applied to guide endogenous cell homing. Overall, building capacity for Mφ modulation and cell recruitment in high-stiffness hydrogels represents a simple and effective strategy that can support high levels of periodontal tissue regeneration. Statement of significance The development of hydrogel-based regenerative therapies centered on the mobilization and stimulation of native cells for therapeutics opens a window toward realizing periodontal endogenous regeneration. In the present study, the parallel use of immunomodulatory and homing factors in high-stiffness hydrogel materials is shown to induce stem cell homing, modulate cell differentiation and indeed induce regrowth of the periodontium. We found that incorporation of interleukin (IL)-4 in high-stiffness TG-gels coaxed macrophages to polarize into M2 phenotypes, and stromal cell-derived factor (SDF)-1α could be applied to direct endogenous cell homing. Hence, we present for the first time a clinically relevant strategy based on macrophage modulation and host cell recruitment that can support high levels of periodontal tissue regeneration.

We build and train an artificial neural network (ANN) model based on experimental α-decay energy (Qα) data. In addition to decays between the ground states of parent and daughter nuclei, decays from the ground states of parent nuclei to the excited states of daughter nuclei are also included. In this way, the number of samples is increased dramatically. The α particle is assumed to have a spherical symmetric shape. The root-mean-square deviation between the calculated results obtained from the ANN model and the experimental data is 0.105 MeV. It shows a good predictive power for α-decay energy with the ANN model. The influence of different inputs is investigated. It is found that both the shell effect and the pairing effect result in an obvious improvement of the predictive power of the ANN model, and the shell effect plays a more important role. The optimal result can be obtained when both the shell and pairing effects are considered simultaneously. The application of the ANN model in predicting α-decay energy indicates a neutron magic number at N=184 in the superheavy nuclei mass region.

Periodontitis is a widespread disease characterized by inflammation-induced progressive damage to the tooth-supporting structures until tooth loss occurs. The regeneration of lost/damaged support tissue in the periodontium, including the alveolar bone, periodontal ligament, and cementum, is an ambitious purpose of periodontal regenerative therapy and might effectively reduce periodontitis-caused tooth loss. The use of stem cells for periodontal regeneration is a hot field in translational research and an emerging potential treatment for periodontitis. This concise review summarizes the regenerative approaches using either culture-expanded or host-mobilized stem cells that are currently being investigated in the laboratory and with preclinical models for periodontal tissue regeneration and highlights the most recent evidence supporting their translational potential toward a widespread use in the clinic for combating highly prevalent periodontal disease. We conclude that in addition to in vitro cell-biomaterial design and transplantation, the engineering of biomaterial devices to encourage the innate regenerative capabilities of the periodontium warrants further investigation. In comparison to cell-based therapies, the use of biomaterials is comparatively simple and sufficiently reliable to support high levels of endogenous tissue regeneration. Thus, endogenous regenerative technology is a more economical and effective as well as safer method for the treatment of clinical patients. Stem Cells Translational Medicine 2019;8:392–403

Background Stem cells that have undergone long-term ex vivo expansion are most likely functionally compromised (namely cellular senescence) in terms of their stem cell properties and therapeutic potential. Due to its ability to attenuate cellular senescence, melatonin (MLT) has been proposed as an adjuvant in long-term cell expansion protocols, but the mechanism underlying MLT-induced cell rejuvenation remains largely unknown. Methods Human periodontal ligament stem cells (PDLSCs) were isolated and cultured ex vivo for up to 15 passages, and cells from passages 2, 7, and 15 (P2, P7, and P15) were used to investigate cellular senescence and autophagy change in response to long-term expansion and indeed the following MLT treatment. Next, we examined whether MLT could induce cell rejuvenation by restoring the autophagic processes of damaged cells and explored the underlying signaling pathways. In this context, cellular senescence was indicated by senescence-associated β-galactosidase (SA-β-gal) activity and by the expression of senescence-related proteins, including p53, p21, p16, and γ-H2AX. In parallel, cell autophagic processes were evaluated by examining autophagic vesicles (by transmission electronic microscopy), autophagic flux (by assessing mRFP-GFP-LC3-transfected cells), and autophagy-associated proteins (by Western blot assay of Atg7, Beclin-1, LC3-II, and p62). Results We found that long-term in vitro passaging led to cell senescence along with impaired autophagy. As expected, MLT supplementation not only restored cells to a younger state but also restored autophagy in senescent cells. Additionally, we demonstrated that autophagy inhibitors could block MLT-induced cell rejuvenation. When the underlying signaling pathways involved were investigated, we found that the MLT receptor (MT) mediated MLT-related autophagy restoration by regulating the PI3K/AKT/mTOR signaling pathway. Conclusions The present study suggests that MLT may attenuate long-term expansion-caused cellular senescence by restoring autophagy, most likely via the PI3K/AKT/mTOR signaling pathway in an MT-dependent manner. This is the first report identifying the involvement of MT-dependent PI3K/AKT/mTOR signaling in MLT-induced autophagy alteration, indicating a potential of autophagy-restoring agents such as MLT to be used in the development of optimized clinical-scale cell production protocols.

A new α-emitting isotope ^{214}U, produced by the fusion-evaporation reaction ^{182}W(^{36}Ar,4n)^{214}U, was identified by employing the gas-filled recoil separator SHANS and the recoil-α correlation technique. More precise α-decay properties of even-even nuclei ^{216,218}U were also measured in the reactions of ^{40}Ar, ^{40}Ca beams with ^{180,182,184}W targets. By combining the experimental data, improved α-decay reduced widths δ^{2} for the even-even Po-Pu nuclei in the vicinity of the magic neutron number N=126 are deduced. Their systematic trends are discussed in terms of the N_{p}N_{n} scheme in order to study the influence of proton-neutron interaction on α decay in this region of nuclei. It is strikingly found that the reduced widths of ^{214,216}U are significantly enhanced by a factor of two as compared with the N_{p}N_{n} systematics for the 84≤Z≤90 and N

The particle-number-conserving (PNC) method in the framework of cranked shell model (CSM) is developed to deal with the reflection-asymmetric nuclear system by applying the ${S}_{x}$ symmetry. Based on an octupole-deformed Nilsson potential, the alternating-parity bands in $^{236,238}\mathrm{U}$ and $^{238,240}\mathrm{Pu}$ are investigated. The experimental kinematic moments of inertia (MoI) and the angular momentum alignments of all studied bands are reproduced well in the PNC-CSM calculations. The striking difference of rotational behaviors between U and Pu isotopes can be linked to the strength of octupole correlations. The upbendings of the alternating-parity bands in $^{236,238}\mathrm{U}$ are due to the alignments of pairs of nucleons occupying $\ensuremath{\nu}{g}_{9/2}, \ensuremath{\pi}{f}_{7/2}$ orbitals and $\ensuremath{\nu}{j}_{15/2}, \ensuremath{\pi}{i}_{13/2}$ high-$j$ intruder orbitals. In particular, the interference terms of nucleon occupying the octupole-correlation pairs of ${\ensuremath{\nu}}^{2}{j}_{15/2}{g}_{9/2}$ and of ${\ensuremath{\pi}}^{2}{i}_{13/2}{f}_{7/2}$ give a very important contribution to the suddenly gained alignments.

Background: Stem cells undergone long-term ex-vivo expansion are most likely functionally compromised (namely cellular senescence) in terms of their stem cell properties and therapeutic potentials. Due to the ability to attenuate cellular senescence, melatonin (MLT) has been proposed as an adjuvant across long-term cell expansion protocols, but the underlying mechanism remains largely unknown. Methods: Human periodontal ligament stem cells (PDLSCs) were isolated and cultured ex-vivo for 15 passages, and passage 2, 7 and 15 cells were used to interrogate the cellular senescence and alteration in cell autophagy during long-term expansion. The cellular senescence features were evidenced by senescence-associated β-galacotosidase (SA-β-gal) activity and the expression of senescence-related proteins including p53, p21, p16 and γ-H2AX. Electronic microscope was used to observe the autophagic vesicles. Adenovirus mRFP-GFP-LC3 was transfected to indicate the alteration of autophagic flux during long-term expansion, and the autophagy-associated proteins Atg7, Beclin-1, LC3-II and p62 were evaluated by Western blot. Results: It was found that long-term in-vitro passaging led to an accumulated SA-β-gal, elevated expressions of p53, p21, p16 and γ-H2AX, along with downregulated autophagy-associated proteins Atg7, Beclin-1 and LC3 as well as a mounting autophagy substrate p62. In accordance with expectation, supplemented with MLT not only ameliorated cells to a younger state but also restored the impaired autophagy level in senescent cells. Additionally, we demonstrated that autophagy inhibitor could block such MLT-induced cell rejuvenation. When the underlying signaling pathways involved was interrogated, we found that MLT receptor (MT) participated in mediating MLT-related autophagy restoration by regulating PI3K/AKT/mTOR signaling pathway.Conclusions: The present study suggests that MLT may rejuvenate long-term expansion-caused cellular senescence by restoring autophagy, more likely via PI3K/AKT/mTOR signaling pathway in an MT-dependent manner. This is the first report identifying the MT-dependent PI3K/AKT/mTOR signaling involved in MLT-induced autophagy alteration, pointing to a potential target for using autophagy-restoring agents such as MLT to develop optimized clinical-scale cell production protocols.

Within the framework of Dyson--Schwinger equations of QCD, we study the effect of finite volume on the chiral phase transition in a sphere with the MIT boundary condition. We find that the chiral quark condensate $\langle\bar�� ��\rangle$ and pseudotransition temperature $T_{pc}$ of the crossover decreases as the volume decreases, until there is no chiral crossover transition at last. We find that the system for $R = \infty $\ fm is indistinguishable from $R=10$ fm and there is a significant decrease in $T_{pc}$ with $R$ as $R, 5 pages, 2 figures

The ground-state bands (GSBs) in the even-even hafnium isotopes $^{170--184}\mathrm{Hf}$ are investigated by using the cranked shell model with pairing correlations treated by the particle-number conserving method. The experimental kinematic moments of inertia are reproduced very well by theoretical calculations. The second upbending of the GSB at high frequency $\ensuremath{\hbar}\ensuremath{\omega}\ensuremath{\approx}0.5$ MeV observed (predicted) in $^{172}\mathrm{Hf}$ ($^{170,174--178}\mathrm{Hf}$) attributes to the sudden alignments of the proton high-$j$ orbitals $\ensuremath{\pi}1{i}_{13/2} (1/{2}^{+}[660]),\phantom{\rule{0.16em}{0ex}}\ensuremath{\pi}1{h}_{9/2} (1/{2}^{\ensuremath{-}}[541])$ and orbital $\ensuremath{\pi}1{h}_{11/2} (7/{2}^{\ensuremath{-}}[523])$. The first upbendings of GSBs at low frequency $\ensuremath{\hbar}\ensuremath{\omega}=0.2--0.3$ MeV in $^{170--178}\mathrm{Hf}$, which locate below the deformed neutron shell $N=108$, attribute to the alignment of the neutron orbital $\ensuremath{\nu}1{i}_{13/2}$. For the heavier even-even isotopes $^{180--184}\mathrm{Hf}$, compared to the lighter isotopes, the first band cross is delayed to the high frequency due to the existence of the deformed shells $N=108,116$. The upbendings of GSBs in $^{180--184}\mathrm{Hf}$ are predicted to occur at $\ensuremath{\hbar}\ensuremath{\omega}\ensuremath{\approx}0.5$ MeV, which come from the sharp raise of the simultaneous alignments of both proton $\ensuremath{\pi}1{i}_{13/2},\phantom{\rule{0.16em}{0ex}}\ensuremath{\pi}1{h}_{9/2}$ and neutron $\ensuremath{\nu}2{g}_{9/2}$ orbitals. The pairing correlation plays a very important role in the rotational properties of GSBs in even-even isotopes $^{180--184}\mathrm{Hf}$. Its effects on upbendings and band-crossing frequencies are investigated.

A new, very short-lived neutron-deficient isotope $^{222}\mathrm{Np}$ was produced in the complete-fusion reaction $^{187}\mathrm{Re}(^{40}\mathrm{Ar},5\mathrm{n})^{222}\mathrm{Np}$, and observed at the gas-filled recoil separator SHANS. The new isotope $^{222}\mathrm{Np}$ was identified by employing a recoil-$\ensuremath{\alpha}$ correlation measurement, and six $\ensuremath{\alpha}$-decay chains were established for it. The decay properties of $^{222}\mathrm{Np}$ with ${E}_{\ensuremath{\alpha}}=10016(33)\text{ }\text{ }\mathrm{keV}$ and ${T}_{1/2}=38{0}_{\ensuremath{-}110}^{+260}\text{ }\text{ }\mathrm{ns}$ were determined experimentally. The $\ensuremath{\alpha}$-decay systematics of Np isotopes is improved by adding the new data for $^{222}\mathrm{Np}$, which validates the $N=126$ shell effect in Np isotopes. The evolution of the $N=126$ shell closure is discussed in the neutron-deficient nuclei up to Np within the framework of $\ensuremath{\alpha}$-decay reduced width.

We study the chirally imbalanced hot and dense strongly interacting matter by means of the Dyson-Schwinger equations (DSEs). The chiral phase diagram is studied in the presence of chiral chemical potential μ 5. The chiral quark condensate ψ ¯ ψ $$ \left\langle \overline{\psi}\psi \right\rangle $$ is obtained with the Cornwall-Jackiw-Tomboulis (CJT) effective action in concert with the Rainbow truncation. Catalysis effect of dynamical chiral symmetry breaking (DCSB) by μ 5 is observed. We examine with two popular gluon models and consistency is found within the DSE approach, as well as in comparison with lattice QCD. The critical end point (CEP) location (μ E , T E ) shifts toward larger T E but constant μ E as μ 5 increases. A technique is then introduced to compute the chiral charge density n 5 from the fully dressed quark propagator. We find the n 5 generally increases with temperature T , quark number chemical potential μ and μ 5. Since the chiral magnetic effect (CME) is typically investigated with peripheral collisions, we also investigate the finite size effect on n 5 and find an increase in n 5 with smaller system size.

Background Robust activation of glial cells has been reported to occur particularly during the pathogenesis of bone cancer pain (BCP). Researchers from our group and others have shown that histone deacetylases (HDACs) play a significant role in modulating glia-mediated immune responses; however, it still remains unclear whether HDACs are involved in the activation of glial cells during the development of BCP. Methods BCP model was established by intra-tibia tumor cell inoculation (TCI). The expression levels and distribution sites of histone deacetylases (HDACs) in the spinal dorsal horn and dorsal root ganglia were evaluated by Western blot and immunofluorescent staining, respectively. Suberoylanilide hydroxamic acid (SAHA), a clinically used HDAC inhibitor, was then intraperitoneally and intrathecally injected to rescue the increased expression levels of HDAC1 and HDAC2. The analgesic effects of SAHA administration on BCP were then evaluated by measuring the paw withdrawal thresholds (PWTs). The effects of SAHA on activation of glial cells and expression of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) in the spinal dorsal horn and dorsal root ganglia of TCI rats were further evaluated by immunofluorescent staining and Western blot analysis. Subsequently, the effects of SAHA administration on tumor growth and cancer cell-induced bone destruction were analyzed by hematoxylin and eosin (HE) staining and micro-CT scanning. Results TCI caused rapid and long-lasting increased expression of HDAC1/HDAC2 in glial cells of the spinal dorsal horn and dorsal root ganglia. Inhibiting HDACs by SAHA not only reversed TCI-induced upregulation of HDACs but also inhibited the activation of glial cells in the spinal dorsal horn and dorsal root ganglia, and relieved TCI-induced mechanical allodynia. Further, we found that SAHA administration could not prevent cancer infiltration or bone destruction in the tibia, which indicated that the analgesic effects of SAHA were not due to its anti-tumor effects. Moreover, we found that SAHA administration could inhibit GSK3β activity in the spinal dorsal horn and dorsal root ganglia, which might contributed to the relief of BCP. Conclusion Our findings suggest that HDAC1 and HDAC2 are involved in the glia-mediated neuroinflammation in the spinal dorsal horn and dorsal root ganglia underlying the pathogenesis of BCP, which indicated that inhibiting HDACs by SAHA might be a potential strategy for pain relief of BCP.

Background Although dental pulp stem cells (DPSCs) isolated from periodontally compromised teeth (P-DPSCs) have been demonstrated to retain pluripotency and regenerative potential, their use as therapeutics remains largely unexplored. In this study, we investigated the proangiogenic effects of extracellular vesicles (EVs) secreted by P-DPSCs using in vitro and in vivo testing models. Methods Patient-matched DPSCs derived from periodontally healthy teeth (H-DPSCs) were used as the control for P-DPSCs. Conditioned media (CMs) derived from H-DPSCs and P-DPSCs (H-CM and P-CM), CMs derived from both cell types pretreated with the EV secretion blocker GW4869 (H-GW and P-GW), and EVs secreted by H-DPSCs and P-DPSCs (H-EVs and P-EVs) were prepared to test their proangiogenic effects on endothelial cells (ECs). Cell proliferation, migration, and tube formation were assessed using the Cell Counting Kit-8 (CCK-8), transwell/scratch wound healing, and Matrigel assays, respectively. Specifically, quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) and western blot analysis were used to examine the expression levels of angiogenesis-related genes/proteins in ECs in response to EV-based incubation. Finally, a full-thickness skin defect model was applied to test the effects of EVs on wound healing and new vessel formation. Results Both H-CM and P-CM promoted EC angiogenesis, but the proangiogenic effects were compromised when ECs were incubated in H-GW and P-GW, wherein the EV secretion was blocked by pretreatment with GW4869. In EV-based incubations, although both H-EVs and P-EVs were found to enhance the angiogenesis-related activities of ECs, P-EVs exerted a more robust potential to stimulate EC proliferation, migration, and tube formation. In addition, P-EVs led to higher expression levels of angiogenesis-related genes/proteins in ECs than H-EVs. Similarly, both P-EVs and H-EVs were found to accelerate wound healing and promote vascularization across skin defects in mice, but wounds treated with P-EVs resulted in a quicker healing outcome and enhanced new vessel formation. Conclusions The findings of the present study provide additional evidence that P-DPSCs derived from periodontally diseased teeth represent a potential source of cells for research and therapeutic use. Particularly, the proangiogenic effects of P-EVs suggest that P-DPSCs may be used to promote new vessel formation in cellular therapy and regenerative medicine.

Although titanium implants have been applied in dental clinics to replace lost teeth and to restore masticatory function for decades, strategies to design the surface of the transmucosal sites of implants to achieve ideal and predictable biological sealing following implantation remain to be optimized. In this study, we hypothesized that gingival epithelial cell (GEC) adhesion and new tissue attachment to titanium sheets/implants could be promoted by the release of plasmid pLAMA3-CM (encoding a motif of the C-terminal globular domain of LAMA3) from a titanium surface. To test this hypothesis, a chitosan/collagen (Chi/Col) coating was immobilized on the surfaces of titanium substrates with nanotube topography (NT-Ti) through cathodic electrophoretic deposition; it was found that pLAMA3-CM could be released from the coating in a highly sustained manner. After culturing on titanium with nanotube topography coated by Chi/Col with the plasmid pLAMA3-CM (Chi/Col/pLAMA3-CM-Ti), human GECs (hGECs) were found to effectively uptake the incorporated plasmids, which resulted in improved attachment, as evidenced by morphological and immunofluorescence analyses. In addition, Chi/Col/pLAMA3-CM-Ti induced better biological sealing at transmucosal sites following immediate implantation into Sprague-Dawley rats. Our findings indicate that the modification of titanium implants by plasmid-mediated pLAMA3-CM gene transfection points to a practical strategy for optimizing biological sealing around the transmucosal sites of implants.

To investigate the effects of vitamin E on the respiratory function impairment in rats with chronic obstructive pulmonary disease (COPD) after exposed to high temperature and PMFifty-four 7-week-old SPF male Wistar rats were randomly divided into 9 experimental groups (n=6). The rat COPD model was established by lipopolysaccharide (LPS) and smoke exposure. After modeled, the rats were tracheal instilled with PMCompared with the control group, exposure of high temperature and PMHigh temperature and PM

Over the past two decades, an accumulating body of evidence indicates that well-designed biomaterials are able to coax the homing of resident stem cells to injured sites and orchestrate their behaviors and functions to promote tissue regeneration. This paradigm opens a new research avenue, termed endogenous regenerative medicine (ERM) in this manuscript, that takes advantage of the body's own regenerative capacity to manage a broad spectrum of ischemic and degenerative diseases. By building on the hidden regenerative potential of resident stem cells, ERM circumvents the complex processes involved in tissue engineering and thereby facilitates the development of clinically translatable regenerative approaches. In fact, tremendous progress has been achieved in the field of ERM, and a large body of literature covering both biological discoveries made in the laboratory and preclinical successes in animal models supports the notion that ERM technologies should be translated to clinical scenarios aimed at curing disease states. In this manuscript, we summarize the strategies with either demonstrated effectiveness or significant potential for harnessing stem cell homing in therapeutics with the aims of defining new criteria for biomaterial design in the field of ERM and predicting future developments in this ever-evolving and rapidly advancing arena.

Although macrophage (Mφ) polarization has been demonstrated to play crucial roles in cellular osteogenesis across the cascade of events in periodontal regeneration, how polarized Mφ phenotypes influence the cementoblastic differentiation of periodontal ligament stem cells (PDLSCs) remains unknown. In the present study, human monocyte leukemic cells (THP-1) were induced into M0, M1, and M2 subsets, and the influences of these polarized Mφs on the cementoblastic differentiation of PDLSCs were assessed in both conditioned medium-based and Transwell-based coculture systems. Furthermore, the potential pathways and cyto-/chemokines involved in Mφ-mediated cementoblastic differentiation were screened and identified. In both systems, M2 subsets increased cementoblastic differentiation-related gene/protein expression levels in cocultured PDLSCs, induced more PDLSCs to differentiate into polygonal and square cells, and enhanced alkaline phosphatase activity in PDLSCs. Furthermore, Akt and c-Jun N-terminal Kinase (JNK) signaling was identified as a potential pathway involved in M2 Mφ-enhanced PDLSC cementoblastic differentiation, and cyto-/chemokines (interleukin (IL)-10 and vascular endothelial growth factor [VEGF]) secreted by M2 Mφs were found to be key players that promoted cell cementoblastic differentiation by activating Akt signaling. Our data indicate for the first time that Mφs are key modulators during PDLSC cementoblastic differentiation and are hence very important for the regeneration of multiple periodontal tissues, including the cementum. Although the Akt and JNK pathways are involved in M2 Mφ-enhanced cementoblastic differentiation, only the Akt pathway can be activated via a cyto-/chemokine-associated mechanism, suggesting that players other than cyto-/chemokines also participate in the M2-mediated cementoblastic differentiation of PDLSCs. Stem Cells 2019;37:1567–1580

Extracellular matrices (ECMs) derived from native tissues/organs have been used as biomaterials for tissue engineering and regenerative medicine in a wide range of preclinical and clinical settings. The success or failure of these applications is largely contingent on the host responses to the matrices in vivo. Despite retaining their native structural and functional proteins, bone ECM-based transplants have been reported to evoke adverse immune responses in many cases; thus, optimizing the immunomodulatory properties of bone ECMs is critical for ensuring downstream regenerative outcomes. Using a simple digestion-neutralization protocol, we transformed the commonly used bone-derived filler particles into gel bioscaffolds. Instead of inducing macrophages toward proinflammatory (M1) polarization, as reported in the literature and confirmed in the present study for ECM particles, the ECM gels were found to be more likely to polarize macrophages toward regulatory/anti-inflammatory (M2) phenotypes, leading to enhanced tissue regeneration in a rat periodontal defect model. The present work demonstrates a simple, practical and economical strategy to modify the immunomodulatory properties of bone ECMs before their in vivo transplantation and hence has important implications that may facilitate the use of ECM-based bioscaffolds derived from diverse sources of tissues for regenerative purposes.

Inspired by the newly discovered isomeric states in the rare-earth neutron-rich nuclei, high-$K$ isomeric states in neutron-rich samarium and gadolinium isotopes are investigated within the framework of the cranked shell model (CSM) with pairing correlation treated by a particle-number-conserving (PNC) method. The experimental multiparticle state energies and moments of inertia are reproduced quite well by the PNC-CSM calculations. A remarkable effect from the high-order deformation ${\ensuremath{\varepsilon}}_{6}$ is demonstrated. Based on the occupation probabilities, the configurations are assigned to the observed high-$K$ isomeric states. The lower ${5}^{\ensuremath{-}}$ isomeric state in $^{158}\mathrm{Sm}$ is preferred as the two-proton state with configuration $\ensuremath{\pi}{\frac{5}{2}}^{+}[413]\ensuremath{\bigotimes}\ensuremath{\pi}{\frac{5}{2}}^{\ensuremath{-}}[532]$. More low-lying two-particle states are predicted. The systematics of the electric quadrupole transition probabilities $B(E2)$ among the neodymium, samarium, gadolinium, and dysprosium isotopes and $N=96,98,100,102$ isotones is investigated to reveal the midshell collectivities.

Increasing evidence indicates that material pore size can affect both macrophage (Mφ) polarization and new vessel formation within the compartment of a transplant. Using genipin cross-linked collagen/chitosan (Col-Ch) scaffolds with average pore sizes of 160 and 360 μm (Col-Ch-160 and Col-Ch-360, respectively) as material vascularization models, this study examined the influence of pore size-mediated M1-to-M2 transition of Mφs penetrating the scaffold on subsequent angiogenesis and vascularization. Following seeding in scaffolds, Mφs (M0 or M1) on both scaffolds tended to exhibit the M1 phenotype at day 1 and the M2 phenotype at day 3 and day 7. Col-Ch-360 exhibited a greater potential to encourage M1-to-M2 transition and to promote Mφ secretion of anti-inflammatory and pro-angiogenic cytokines. When supernatants derived from Mφ-scaffold cultures were used to incubate human umbilical vein endothelial cells (HUVECs), cells incubated with Col-Ch-360-derived supernatants displayed a great angiogenic response in terms of tube formation and cell migration. Compared with Col-Ch-160, subcutaneous transplantation of Col-Ch-360 scaffolds resulted in more blood vessel formation, along with more VEGF+ cells and fewer pro-inflammatory (M1) Mφs across the pores of the material. Our data suggest that compared to Col-Ch-160, Col-Ch-360 scaffolds promote angiogenesis in vitro and vascularization in vivo, most likely because Mφs residing in materials with larger pores undergo a higher degree of M1-to-M2 transition.

The multi-particle states and rotational properties of the two-particle bands in are investigated by the cranked shell model with pairing correlations treated by the particle number conserving method. The rotational bands on top of the two-particle and states and the pairing reduction are studied theoretically in for the first time. The experimental excitation energies and moments of inertia of the multi-particle states are reproduced well by the calculations. Better agreement with the data is achieved by including the high-order deformation , which leads to enlarged and deformed shell gaps. An increase of in these two-particle bands compared with the ground state band is attributed to the pairing reduction due to the Pauli blocking effect.

Experimentally observed superdeformed (SD) rotational bands in $^{36}$Ar and $^{40}$Ar are studied by the cranked shell model (CSM) with the paring correlations treated by a particle-number-conserving (PNC) method. This is the first time the PNC-CSM calculations are performed on the light nuclear mass region around $A=40$. The experimental kinematic moments of inertia $J^{(1)}$ versus rotational frequency are reproduced well. The backbending of the SD band at frequency around $\hbar\omega=1.5$ MeV in $^{36}$Ar is attributed to the sharp rise of the simultaneous alignments of the neutron and proton $1d_{5/2}[202]5/2$ pairs and $1f_{7/2}[321]3/2$ pairs, which is the consequence of the band crossing between the $1d_{5/2}[202]5/2$ and $1f_{7/2}[321]3/2$ configuration states. The gentle upbending at the low frequency of the SD band in $^{40}$Ar is mainly effected by the alignments of the neutron $1f_{7/2}[321]3/2$ pairs and proton $1d_{5/2}[202]5/2$ pairs. The PNC-CSM calculations show that besides the diagonal parts, the off-diagonal parts of the alignments play an important role in the rotational behavior of the SD bands.

Macrophages (Mφs) are involved in a variety of physiological and pathological events including wound healing and tissue regeneration, in which they play both positive and negative roles depending on their polarization state. In this study, we investigated the cellular behaviours of bone marrow mesenchymal stem cells (BMMSCs) after incubation in different conditioned media (CMs) generated by unpolarized Mφs (M0) or polarized Mφs (M1 and M2). Mφ polarization was induced by stimulation with various cytokines, and CMs were obtained from in vitro Mφ cultures termed CM0, CM1 and CM2 based on each Mφ phenotype. We found that CM1 supported the proliferation and adipogenic differentiation of BMMSCs, whereas CM0 had a remarkable effect on cell osteogenic differentiation. To a certain degree, CM2 also facilitated BMMSC osteogenesis; in particular, cells incubated with CM2 exhibited an enhanced capacity to form robust stem cell sheets. Although incubation with CM1 also increased production of extracellular matrix components, such as fibronectin, COL‐1 and integrin β1during sheet induction, the sheets generated by CM2‐incubated cells were thicker than those generated by CM1‐incubated cells (P < 0.001). Our data suggest that each Mφ phenotype has a unique effect on BMMSCs. Fine‐tuning Mφ polarization following transplantation may serve as an effective method to modulate the therapeutic potential of BMMSCs.

Accumulating evidence indicates that the physicochemical properties of biomaterials exert profound influences on stem cell fate decisions. However, matrix-based regulation selected through in vitro analyses based on a given cell population do not genuinely reflect the in vivo conditions, in which multiple cell types are involved and interact dynamically. This study constitutes the first investigation of how macrophages (Mφs) in stiffness-tunable transglutaminase cross-linked gelatin (TG-gel) affect the osteogenesis of bone marrow-derived mesenchymal stem cells (BMMSCs). When a single cell type was cultured, low-stiffness TG-gels promoted BMMSC proliferation, whereas high-stiffness TG-gels supported cell osteogenic differentiation. However, Mφs in high-stiffness TG-gels were more likely to polarize toward the pro-inflammatory M1 phenotype. Using either conditioned medium (CM)-based incubation or Transwell-based co-culture, we found that Mφs encapsulated in the low-stiffness matrix exerted a positive effect on the osteogenesis of co-cultured BMMSCs. Conversely, Mφs in high-stiffness TG-gels negatively affected cell osteogenic differentiation. When both cell types were cultured in the same TG-gel type and placed into the Transwell system, the stiffness-related influences of Mφs on BMMSCs were significantly altered; both the low- and high-stiffness matrix induced similar levels of BMMSC osteogenesis. Although the best material parameter for synergistically affecting Mφs and BMMSCs remains unknown, our data suggest that Mφ involvement in the co-culture system alters previously identified material-related influences on BMMSCs, such as matrix stiffness-related effects, which were identified based on a culture system involving a single cell type. Such Mφ-stem cell interactions should be considered when establishing proper matrix parameter-associated cell regulation in the development of biomimetic biomaterials for regenerative applications. Statement of Significance The substrate stiffness of a scaffold plays critical roles in modulating both reparative cells, such as mesenchymal stem cells (MSCs), and immune cells, such as macrophages (Mφs). Although the influences of material stiffness on either Mφs or MSCs, have been extensively described, how the two cell types respond to matrix cues to dynamically affect each other in a three-dimensional (3D) biosystem remains largely unknown. Here, we report our findings that, in a platform wherein Mφs and bone marrow-derived MSCs coexist, matrix stiffness can influence stem cell fate through both direct matrix-associated regulation and indirect Mφ-based modulation. Our data support future studies of the MSC-Mφ-matrix interplay in the 3D context to optimize matrix parameters for the development of the next biomaterial.

Resident stem cell pools in many tissues/organs are responsible not only for tissue maintenance during physiologic turnover but also for the process of wound repair following injury. With inspiration from stem cell trafficking within the body under physiologic and pathologic conditions, recent advances have been made toward inducing stem cell mobilization and directing patients’ own cells to sites of interest for treating a broad spectrum of diseases. An evolving body of work corroborates that delivering guidance cues can mobilize stem cells from the bone marrow and drive these cells toward a specific region. In addition, the transplantation of cell-friendly biomaterials incorporating certain biomolecules has led to the regeneration of lost/damaged tissue without the need for delivering cellular materials manipulated ex vivo. Recently, cell homing has resulted in remarkable biological discoveries in the laboratory as well as great curative successes in preclinical scenarios. Here, we review the biological evidence underlying in vivo cell mobilization and homing with the aim of leveraging endogenous reparative cells for therapeutic applications. Considering both the promise and the obstacles of this approach, we discuss how matrix components of the in vivo milieu can be modified to promote the native regenerative process and inspire future tissue-engineering design.

The use of stem cell-derived sheets has become increasingly common in a wide variety of biomedical applications. Although substantial evidence has demonstrated that human platelet lysate (PL) can be used for therapeutic cell expansion, either as a substitute for or as a supplement to xenogeneic fetal bovine serum (FBS), its impact on cell sheet production remains largely unexplored. In this study, we manufactured periodontal ligament stem cell (PDLSC) sheets in vitro by incubating PDLSCs in sheet-induction media supplemented with various ratios of PL and FBS, i.e. 10% PL without FBS, 7.5% PL + 2.5% FBS, 5% PL + 5% FBS, 2.5% PL + 7.5% FBS or 10% FBS without PL. Cultures with the addition of all the designed supplements led to successful cell sheet production. In addition, all the resultant cellular materials exhibited similar expression profiles of matrix-related genes and proteins, such as collagen I, fibronectin and integrin β1. Interestingly, the cell components within sheets generated by media containing both PL and FBS exhibited improved osteogenic potential. Following in vivo transplantation, all sheets supported significant new bone formation. Our data suggest that robust PDLSC sheets can be produced by applying PL as either an alternative or an adjuvant to FBS. Further examination of the relevant influences of human PL that benefit cell behaviour and matrix production will pave the way towards optimized and standardized conditions for cell sheet production.

Ex vivo‐expanded stem cells have long been a cornerstone of biotherapeutics and have attracted increasing attention for treating intractable diseases and improving tissue regeneration. However, using exogenous cellular materials to develop restorative treatments for large numbers of patients has become a major concern for both economic and safety reasons. Advances in cell biological research over the past two decades have expanded the potential for using endogenous stem cells during wound healing processes, and in particular, recent insight into stem cell movement and homing has prompted regenerative research and therapy based on recruiting endogenous cells. Inspired by the natural healing process, artificial administration of specific chemokines as signals systemically or at the injury site, typically using biomaterials as vehicles, is a state‐of‐the‐art strategy that potentiates stem cell homing and recreates an anti‐inflammatory and immunomodulatory microenvironment to enhance in situ tissue regeneration. However, pharmacologically coaxing endogenous stem cells to act as therapeutics in the field of biomedicine remains in the early stages; its efficacy is limited by the lack of innovative methodologies for chemokine presentation and release. This review describes how to direct the homing of endogenous stem cells via the administration of specific signals, with a particular emphasis on targeted signalling molecules that regulate this homing process, to enhance in situ tissue regeneration. We also provide an outlook on and critical considerations for future investigations to enhance stem cell recruitment and harness the reparative potential of these recruited cells as a clinically relevant cell therapy.

The lateral capsular division of central nucleus of amygdala (CeC) contains neurons using γ-amino butyric acid (GABA) as the predominant neurotransmitter and expresses abundant calcitonin gene-related peptide (CGRP)-positive terminals. However, the relationship between them has not been revealed yet. Using GAD67-green fluorescent protein (GFP) knock-in mouse, we investigated the neurochemical features of synapses between CGRP-positive terminals and GABAergic neurons within CeC and the potential involvement of CGRP1 receptor by combining fluorescent in situ hybridization for CGRP1 receptor mRNA with immunofluorescent histochemistry for GFP and CGRP. The ultrastructures of these synapses were investigated with pre-embedding electron microscopy for GFP and CGRP. We found that some GABAergic neurons in the CeC received parabrachial nucleus (PBN) derived CGRP innervations and some of these GABAergic neurons can be activated by subcutaneous injection of formalin. Moreover, more than 90 % GABAergic neurons innervated by CGRP-positive terminal also express CGRP1 receptor mRNA. The CGRP-positive fibers made symmetric synapses onto the GABAergic somata, and asymmetric synapses onto the GABA-LI dendritic shafts and spines. This study provides direct ultrastructural evidences for the synaptic contacts between CGRP-positive terminals and GABAergic neurons within the CeC, which may underlie the pain-related neural pathway from PBN to CeC and be involved in the chronic pain modulation.

Experimentally observed ground state band based on the $1/2^{-}[521]$ Nilsson state and the first exited band based on the $7/2^{-}[514]$ Nilsson state in the odd-$Z$ nucleus $^{255}$Lr are studied by the cranked shell model (CSM) with the paring correlations treated by the particle-number-conserving (PNC) method. This is the first time the detailed theoretical investigations being performed on these rotational bands. Both the experimental kinematic and dynamic moment of inertia ($\mathcal{J}^{(1)}$ and $\mathcal{J}^{(2)}$) versus rotational frequency are reproduced quite well by the PNC-CSM calculations. By comparing the theoretical kinematic moment of inertia $\mathcal{J}^{(1)}$ with the experimental ones extracted from different spin assignments, the spin $17/2^{-}\rightarrow13/2^{-}$ is assigned to the lowest-lying $196.6(5)$ keV transition of the $1/2^{-}[521]$ band, and $15/2^{-}\rightarrow11/2^{-}$ to the $189(1)$ keV transition of the $7/2^{-}[514]$ band, respectively. The proton $N=7$ major shell is included in the calculations. The intruder of the high$-j$ low$-\Omega$ orbitals $1j_{15/2}$ $ (1/2^{-}[770])$ at the high spin leads to the band-crossing at $\hbar\omega\approx0.20$ ($\hbar\omega\approx0.25$) MeV for the $7/2^{-}[514]$ $\alpha=-1/2$ ($\alpha=+1/2$) band, and at $\hbar\omega\approx0.175$ MeV for the $1/2^{-}[521]$ $\alpha=-1/2$ band, respectively. Further investigations show that the band-crossing frequencies are quadrupole deformation dependent., Comment: arXiv admin note: text overlap with arXiv:1208.1156 by other authors

The fills of barrier dams commonly result from high-speed landslides debris flow. In this paper, four model tests were conducted to study the effect of fill size on the stability of barrier dams. The failure time, failure mode, pore pressures and earth pressures were then observed and analyzed. The results show that barrier dams composed of coarse-grains or well-graded fills are more stable than those composed of fine-grained fills; coarse-grain-dams are more sensitive to the rising of water level than fine-grain-dams; the failure mode of coarse-grain-dams is usually overflowing-erosion and the barrier dams usually fail from the top of dams; the failure mode of fine-grain-dams is sliding and the barrier dams fail initially from the slope downstream.

National Natural Science Foundation of China[10705014, 10535010, 10775068, 10675006]; CAS Knowledge Innovation[KJCX2-SW-N02]