Let j, k and m be three positive integers, a circular m-L（j, k）-labeling of a graph G is a mapping f： V（G）→{0, 1, …, m-1}such that f（u）-f（v）m≥j if u and v are adjacent, and f（u）-f（v）m≥k if u and v are...Let j, k and m be three positive integers, a circular m-L（j, k）-labeling of a graph G is a mapping f： V（G）→{0, 1, …, m-1}such that f（u）-f（v）m≥j if u and v are adjacent, and f（u）-f（v）m≥k if u and v are at distance two,where a-bm=min{a-b,m-a-b}. The minimum m such that there exists a circular m-L（j, k）-labeling of G is called the circular L（j, k）-labeling number of G and is denoted by σj, k（G）. For any two positive integers j and k with j≤k,the circular L（j, k）-labeling numbers of trees, the Cartesian product and the direct product of two complete graphs are determined.展开更多
An L(h,k)-labeling of a graph G is an assignment of non-negative integers to the vertices such that if two vertices u and v are adjacent then they receive labels that differ by at least h, and when u and v are not adj...An L(h,k)-labeling of a graph G is an assignment of non-negative integers to the vertices such that if two vertices u and v are adjacent then they receive labels that differ by at least h, and when u and v are not adjacent but there is a two-hop path between them, then they receive labels that differ by at least k. The span λ of such a labeling is the difference between the largest and the smallest vertex labels assigned. Let λ<sub>h</sub>k</sup> ( G )denote the least λ such that G admits an L(h,k) -labeling using labels from {0,1,...λ}. A Cayley graph of group is called circulant graph of order n, if the group is isomorphic to Z<sub>n.</sub> In this paper, initially we investigate the L(h,k) -labeling for circulant graphs with “large” connection sets, and then we extend our observation and find the span of L(h,k) -labeling for any circulants of order n. .展开更多
Some studies have confirmed the neuroprotective effect of remote ischemic conditioning against stroke. Although numerous animal researches have shown that the neuroprotective effect of remote ischemic conditioning may...Some studies have confirmed the neuroprotective effect of remote ischemic conditioning against stroke. Although numerous animal researches have shown that the neuroprotective effect of remote ischemic conditioning may be related to neuroinflammation, cellular immunity, apoptosis, and autophagy, the exact underlying molecular mechanisms are unclear. This review summarizes the current status of different types of remote ischemic conditioning methods in animal and clinical studies and analyzes their commonalities and differences in neuroprotective mechanisms and signaling pathways. Remote ischemic conditioning has emerged as a potential therapeutic approach for improving stroke-induced brain injury owing to its simplicity, non-invasiveness, safety, and patient tolerability. Different forms of remote ischemic conditioning exhibit distinct intervention patterns, timing, and application range. Mechanistically, remote ischemic conditioning can exert neuroprotective effects by activating the Notch1/phosphatidylinositol 3-kinase/Akt signaling pathway, improving cerebral perfusion, suppressing neuroinflammation, inhibiting cell apoptosis, activating autophagy, and promoting neural regeneration. While remote ischemic conditioning has shown potential in improving stroke outcomes, its full clinical translation has not yet been achieved.展开更多
A k-L(2,1)-labeling for a graph G is a function such that whenever and whenever u and v are at distance two apart. The λ-number for G, denoted by λ(G), is the minimum k over all k-L(2,1)-labelings of G. In this pape...A k-L(2,1)-labeling for a graph G is a function such that whenever and whenever u and v are at distance two apart. The λ-number for G, denoted by λ(G), is the minimum k over all k-L(2,1)-labelings of G. In this paper, we show that for or 11, which confirms Conjecture 6.1 stated in [X. Li, V. Mak-Hau, S. Zhou, The L(2,1)-labelling problem for cubic Cayley graphs on dihedral groups, J. Comb. Optim. (2013) 25: 716-736] in the case when or 11. Moreover, we show that? if 1) either (mod 6), m is odd, r = 3, or 2) (mod 3), m is even (mod 2), r = 0.展开更多
Cerebral edema caused by blood-brain barrier injury after intracerebral hemorrhage is an important factor leading to poor prognosis.Human-induced pluripotent stem cell-derived neural stem cell exosomes(hiPSC-NSC-Exos)...Cerebral edema caused by blood-brain barrier injury after intracerebral hemorrhage is an important factor leading to poor prognosis.Human-induced pluripotent stem cell-derived neural stem cell exosomes(hiPSC-NSC-Exos)have shown potential for brain injury repair in central nervous system diseases.In this study,we explored the impact of hiPSC-NSC-Exos on blood-brain barrier preservation and the underlying mechanism.Our results indicated that intranasal delivery of hiPSC-NSC-Exos mitigated neurological deficits,enhanced blood-brain barrier integrity,and reduced leukocyte infiltration in a mouse model of intracerebral hemorrhage.Additionally,hiPSC-NSC-Exos decreased immune cell infiltration,activated astrocytes,and decreased the secretion of inflammatory cytokines like monocyte chemoattractant protein-1,macrophage inflammatory protein-1α,and tumor necrosis factor-αpost-intracerebral hemorrhage,thereby improving the inflammatory microenvironment.RNA sequencing indicated that hiPSC-NSC-Exo activated the PI3K/AKT signaling pathway in astrocytes and decreased monocyte chemoattractant protein-1 secretion,thereby improving blood-brain barrier integrity.Treatment with the PI3K/AKT inhibitor LY294002 or the monocyte chemoattractant protein-1 neutralizing agent C1142 abolished these effects.In summary,our findings suggest that hiPSC-NSC-Exos maintains blood-brain barrier integrity,in part by downregulating monocyte chemoattractant protein-1 secretion through activation of the PI3K/AKT signaling pathway in astrocytes.展开更多
Human neural stem cell-derived extracellular vesicles exhibit analogous functions to their parental cells,and can thus be used as substitutes for stem cells in stem cell therapy,thereby mitigating the risks of stem ce...Human neural stem cell-derived extracellular vesicles exhibit analogous functions to their parental cells,and can thus be used as substitutes for stem cells in stem cell therapy,thereby mitigating the risks of stem cell therapy and advancing the frontiers of stem cell-derived treatments.This lays a foundation for the development of potentially potent new treatment modalities for ischemic stroke.However,the precise mechanisms underlying the efficacy and safety of human neural stem cell-derived extracellular vesicles remain unclear,presenting challenges for clinical translation.To promote the translation of therapy based on human neural stem cell-derived extracellular vesicles from the bench to the bedside,we conducted a comprehensive preclinical study to evaluate the efficacy and safety of human neural stem cell-derived extracellular vesicles in the treatment of ischemic stroke.We found that administration of human neural stem cell-derived extracellular vesicles to an ischemic stroke rat model reduced the volume of cerebral infarction and promoted functional recovery by alleviating neuronal apoptosis.The human neural stem cell-derived extracellular vesicles reduced neuronal apoptosis by enhancing phosphorylation of phosphoinositide 3-kinase,mammalian target of rapamycin,and protein kinase B,and these effects were reversed by treatment with a phosphoinositide 3-kinase inhibitor.These findings suggest that human neural stem cell-derived extracellular vesicles play a neuroprotective role in ischemic stroke through activation of phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin signaling pathway.Finally,we showed that human neural stem cell-derived extracellular vesicles have a good in vivo safety profile.Therefore,human neural stem cell-derived extracellular vesicles are a promising potential agent for the treatment of ischemic stroke.展开更多
基金The National Natural Science Foundation of China(No.10971025)
文摘Let j, k and m be three positive integers, a circular m-L（j, k）-labeling of a graph G is a mapping f： V（G）→{0, 1, …, m-1}such that f（u）-f（v）m≥j if u and v are adjacent, and f（u）-f（v）m≥k if u and v are at distance two,where a-bm=min{a-b,m-a-b}. The minimum m such that there exists a circular m-L（j, k）-labeling of G is called the circular L（j, k）-labeling number of G and is denoted by σj, k（G）. For any two positive integers j and k with j≤k,the circular L（j, k）-labeling numbers of trees, the Cartesian product and the direct product of two complete graphs are determined.
文摘An L(h,k)-labeling of a graph G is an assignment of non-negative integers to the vertices such that if two vertices u and v are adjacent then they receive labels that differ by at least h, and when u and v are not adjacent but there is a two-hop path between them, then they receive labels that differ by at least k. The span λ of such a labeling is the difference between the largest and the smallest vertex labels assigned. Let λ<sub>h</sub>k</sup> ( G )denote the least λ such that G admits an L(h,k) -labeling using labels from {0,1,...λ}. A Cayley graph of group is called circulant graph of order n, if the group is isomorphic to Z<sub>n.</sub> In this paper, initially we investigate the L(h,k) -labeling for circulant graphs with “large” connection sets, and then we extend our observation and find the span of L(h,k) -labeling for any circulants of order n. .
基金supported partly by the National Natural Science Foundation of China,No.82071332the Chongqing Natural Science Foundation Joint Fund for Innovation and Development,No.CSTB2023NSCQ-LZX0041 (both to ZG)。
文摘Some studies have confirmed the neuroprotective effect of remote ischemic conditioning against stroke. Although numerous animal researches have shown that the neuroprotective effect of remote ischemic conditioning may be related to neuroinflammation, cellular immunity, apoptosis, and autophagy, the exact underlying molecular mechanisms are unclear. This review summarizes the current status of different types of remote ischemic conditioning methods in animal and clinical studies and analyzes their commonalities and differences in neuroprotective mechanisms and signaling pathways. Remote ischemic conditioning has emerged as a potential therapeutic approach for improving stroke-induced brain injury owing to its simplicity, non-invasiveness, safety, and patient tolerability. Different forms of remote ischemic conditioning exhibit distinct intervention patterns, timing, and application range. Mechanistically, remote ischemic conditioning can exert neuroprotective effects by activating the Notch1/phosphatidylinositol 3-kinase/Akt signaling pathway, improving cerebral perfusion, suppressing neuroinflammation, inhibiting cell apoptosis, activating autophagy, and promoting neural regeneration. While remote ischemic conditioning has shown potential in improving stroke outcomes, its full clinical translation has not yet been achieved.
文摘A k-L(2,1)-labeling for a graph G is a function such that whenever and whenever u and v are at distance two apart. The λ-number for G, denoted by λ(G), is the minimum k over all k-L(2,1)-labelings of G. In this paper, we show that for or 11, which confirms Conjecture 6.1 stated in [X. Li, V. Mak-Hau, S. Zhou, The L(2,1)-labelling problem for cubic Cayley graphs on dihedral groups, J. Comb. Optim. (2013) 25: 716-736] in the case when or 11. Moreover, we show that? if 1) either (mod 6), m is odd, r = 3, or 2) (mod 3), m is even (mod 2), r = 0.
基金supported by the National Natural Science Foundation of China,No.8227050826(to PL)Tianjin Science and Technology Bureau Foundation,No.20201194(to PL)Tianjin Graduate Research and Innovation Project,No.2022BKY174(to CW).
文摘Cerebral edema caused by blood-brain barrier injury after intracerebral hemorrhage is an important factor leading to poor prognosis.Human-induced pluripotent stem cell-derived neural stem cell exosomes(hiPSC-NSC-Exos)have shown potential for brain injury repair in central nervous system diseases.In this study,we explored the impact of hiPSC-NSC-Exos on blood-brain barrier preservation and the underlying mechanism.Our results indicated that intranasal delivery of hiPSC-NSC-Exos mitigated neurological deficits,enhanced blood-brain barrier integrity,and reduced leukocyte infiltration in a mouse model of intracerebral hemorrhage.Additionally,hiPSC-NSC-Exos decreased immune cell infiltration,activated astrocytes,and decreased the secretion of inflammatory cytokines like monocyte chemoattractant protein-1,macrophage inflammatory protein-1α,and tumor necrosis factor-αpost-intracerebral hemorrhage,thereby improving the inflammatory microenvironment.RNA sequencing indicated that hiPSC-NSC-Exo activated the PI3K/AKT signaling pathway in astrocytes and decreased monocyte chemoattractant protein-1 secretion,thereby improving blood-brain barrier integrity.Treatment with the PI3K/AKT inhibitor LY294002 or the monocyte chemoattractant protein-1 neutralizing agent C1142 abolished these effects.In summary,our findings suggest that hiPSC-NSC-Exos maintains blood-brain barrier integrity,in part by downregulating monocyte chemoattractant protein-1 secretion through activation of the PI3K/AKT signaling pathway in astrocytes.
基金supported by the National Nature Science Foundation of China,No.81471308(to JL)the Innovative Leading Talents of Liaoning Province,No.XLYC1902031(to JL)+2 种基金Science and Technology Projects in Liaoning Province,No.2022-BS-238(to CH)Young Top Talents of Liaoning Province,No.XLYC1907009(to LW)Dalian Science and Technology Innovation Fund,No.2018J11CY025(to JL)。
文摘Human neural stem cell-derived extracellular vesicles exhibit analogous functions to their parental cells,and can thus be used as substitutes for stem cells in stem cell therapy,thereby mitigating the risks of stem cell therapy and advancing the frontiers of stem cell-derived treatments.This lays a foundation for the development of potentially potent new treatment modalities for ischemic stroke.However,the precise mechanisms underlying the efficacy and safety of human neural stem cell-derived extracellular vesicles remain unclear,presenting challenges for clinical translation.To promote the translation of therapy based on human neural stem cell-derived extracellular vesicles from the bench to the bedside,we conducted a comprehensive preclinical study to evaluate the efficacy and safety of human neural stem cell-derived extracellular vesicles in the treatment of ischemic stroke.We found that administration of human neural stem cell-derived extracellular vesicles to an ischemic stroke rat model reduced the volume of cerebral infarction and promoted functional recovery by alleviating neuronal apoptosis.The human neural stem cell-derived extracellular vesicles reduced neuronal apoptosis by enhancing phosphorylation of phosphoinositide 3-kinase,mammalian target of rapamycin,and protein kinase B,and these effects were reversed by treatment with a phosphoinositide 3-kinase inhibitor.These findings suggest that human neural stem cell-derived extracellular vesicles play a neuroprotective role in ischemic stroke through activation of phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin signaling pathway.Finally,we showed that human neural stem cell-derived extracellular vesicles have a good in vivo safety profile.Therefore,human neural stem cell-derived extracellular vesicles are a promising potential agent for the treatment of ischemic stroke.
