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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.

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

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.

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

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.

Based on the relativistic calculations of the nuclear masses in the transfermium region from No \begin{document}$ (Z = 102) $\end{document} to Ds \begin{document}$ (Z = 110) $\end{document} using the deformed relativistic Hartree-Bogoliubov theory in continuum (DRHBc), the possible existence of bound nuclei beyond the neutron drip lines is studied. The two-neutron and multi-neutron emission bound nuclei beyond the primary neutron drip line of \begin{document}$ N = 258 $\end{document} are predicted in \begin{document}$ Z = 106,108 $\end{document} , and \begin{document}$ 110 $\end{document} isotopes. A detailed microscopic mechanism investigation reveals that nuclear deformation plays a vital role in the existence of bound nuclei beyond the drip line. Furthermore, not only the quadrupole deformation \begin{document}$ \beta_{2} $\end{document} but also the higher orders of deformation are indispensable in the reliable description of the phenomenon of reentrant binding.

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

Objectives Previously, our investigations demonstrated robust pro‐angiogenic potentials of extracellular vesicles secreted by periodontitis‐compromised dental pulp stem cells (P‐EVs) when compared to those from healthy DPSCs (H‐EVs), but the underlying mechanism remains unknown. Materials and methods Here, circulating microRNAs (miRNAs) specifically found in P‐EVs (compared with H‐EVs) were identified by Agilent miRNA microarray analysis, and the roles of the candidate miRNA in P‐EV‐enhanced cell angiogenesis were confirmed by cell transfection and RNA interference methods. Next, the direct binding affinity between the candidate miRNA and its target gene was evaluated by luciferase reporter assay. CCK‐8, transwell/scratch wound healing and tube formation assays were established to investigate the proliferation, migration, and tube formation abilities of endothelial cells (ECs). Western blot was employed to measure the protein levels of Hedgehog/Gli1 signalling pathway components and angiogenesis‐related factors. Results The angiogenesis‐related miRNA miR‐378a was found to be enriched in P‐EVs, and its role in P‐EV‐enhanced cell angiogenesis was confirmed, wherein Sufu was identified as a downstream target gene of miR‐378a. Functionally, silencing of Sufu stimulated EC proliferation, migration and tube formation by activating Hedgehog/Gli1 signalling. Further, we found that incubation with P‐EVs enabled the transmission of P‐EV‐contained miR‐378a to ECs. Subsequently, the expressions of Sufu, Gli1 and vascular endothelial growth factor in ECs were significantly influenced by P‐EV‐mediated miR‐378a transmission. Conclusions These data suggest that P‐EVs carrying miR‐378a promote EC angiogenesis by downregulating Sufu to activate the Hedgehog/Gli1 signalling pathway. Our findings reveal a crucial role for EV‐derived miR‐378a in cell angiogenesis and hence offer a new target for modifying stem cells and their secreted EVs to enhance vessel regenerative potential., P‐EVs carrying miR‐378a promote the angiogenesis of ECs by down‐regulating Sufu to activate the Hedgehog/Gli1 signalling pathway.

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.

Accumulating evidence indicates that the pluripotency of periodontal ligament stem cells (PDLSCs) is compromised under inflammatory conditions; however, the underlying mechanisms remain largely unexplored. In this study, we hypothesize that the P2X7 receptor (P2X7R) is a key molecule linked to inflammation-associated impairment of PDLSCs. We first investigated P2X7R expression in PDLSCs under normal and inflammatory conditions and then determined the effect of a P2X7R agonist (BzATP) or antagonist (BBG) on PDLSC osteogenesis under various conditions. Gene-modified PDLSCs were used to further examine the role of P2X7R and the signaling pathway underlying P2X7R-enhanced osteogenesis. We found that inflammatory conditions decreased P2X7R expression in PDLSCs and reduced osteogenesis in these cells. In addition, activation of P2X7R by BzATP or overexpression of P2X7R via gene transduction reversed the inflammation-mediated decrease in PDLSC osteogenic differentiation. When selected osteogenesis-related signaling molecules were screened, the PI3K-AKT-mTOR pathway was identified as potentially involved in P2X7R-enhanced PDLSC osteogenesis. Our data reveal a crucial role for P2X7R in PDLSC osteogenesis under inflammatory conditions, suggesting a new therapeutic target to reverse or rescue inflammation-mediated changes in PDLSCs for future mainstream therapeutic uses.

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

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.

We study the chiral phase transition inside a rotating cylinder within the framework of the Nambu--Jona-Lasinio model. A spectral boundary condition is imposed to avoid faster than light. We investigate how the geometry of the cylinder and rotation influence the chiral phase transition at finite temperature and chemical potential. The inhomogeneous effects caused by the finite size and rotation are also taken into account. It is found that finite size will reduce the chiral transition temperature and raises the chiral transition chemical potential, while the rotation reduces both the chiral transition temperature and chemical potential. In addition, we discuss the implications of our results in heavy-ion collisions and equation of states of neutron star.

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.

The aim of this work is to develop the deformed relativistic Hartree-Bogoliubov theory in continuum (DRHBc) theory based on the point-coupling density functionals and extend it to provide a unified description for all even-even nuclei in the nuclear chart by overcoming all possible challenges. The nuclear superfluidity is considered via Bogoliubov transformation. Densities and potentials are expanded in terms of Legendre polynomials to include the axial deformation degrees of freedom. Sophisticated relativistic Hartree-Bogoliubov equations in coordinate space are solved in the DiracWoods-Saxon basis to consider the continuum effects. Numerical checks are performed from light nuclei to heavy nuclei. The techniques to construct the DRHBc mass table for even-even nuclei are explored. The DRHBc theory is extended to study heavier nuclei beyond magnesium isotopes. Taking Nd isotopes as examples, the experimental binding energies, two-neutron separation energies, quadrupole deformations, and charge radii are reproduced rather well. The deformation and continuum play essential roles in the description of nuclear masses and prediction of drip-line nuclei. By examining the single-particle levels in the canonical basis and their contributions to the total density, the thickness of the neutron skin, the particles number in continuum, and the Coulomb barrier, the exotic structures including the neutron skin and the proton radioactivity are predicted., 45 pages, 17 figures, and 1 table, accepted version for Physical Review C

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.