The Tur\'an number of special linear forest and star-path forest

The Tur\'an number of a graph $F$, denoted $ex(n, F)$, is the maximum number of edges in an $F$-free graph on $n$ vertices. Let $P_{\ell}$, $S_{\ell}$ denote the path and star on $\ell$ vertices, respectively. A linear forest is a forest whose connected components are paths. In 2013, Lidick\'y et al. considered the Tur\'an number of linear forest and $k_1P_4 \bigcup k_2 S_3$ for sufficiently large $n$. Recently, Fang and Yuan determine the Tur\'an numbers of $P_{\ell} \bigcup kS_{\ell-1}$, $k_1P_{2\ell} \bigcup k_2 S_{2\ell-1}$, $2P_5 \bigcup kS_4$ for $n$ appropriately large and characterized the corresponding extremal graphs. In this paper, We determine $ex(n, P_9 \bigcup P_7)$ for all $n\geq 16$ and characterize all extremal graphs, which partially confirms a conjecture proposed by Yuan and Zhang [L.T. Yuan, X.D. Zhang, J. Graph. Theory 98(3) (2021) 499--524]. And we determine the Tur\'an numbers of $\bigcup\limits _{i=1}^{k_1} P_{\ell _i} \bigcup\limits _{j=1}^{k_2} S_{a _j}$ for $n$ appropriately large, where $a_j\leq 2k_2+2 \sum\limits_{i=1}^{k_1} \lfloor\frac{\ell_i}{2}\rfloor-2j$ for any $j\in [k_2]$, which generalizes the results of Fang and Yuan. The corresponding extremal graphs are also completely characterizedComment: arXiv admin note: substantial text overlap with arXiv:1711.07734 by other author

Regular graphs with a complete bipartite graph as a star complement

Let $G$ be a graph of order $n$ and $\mu$ be an adjacency eigenvalue of $G$ with multiplicity $k\geq 1$. A star complement $H$ for $\mu$ in $G$ is an induced subgraph of $G$ of order $n-k$ with no eigenvalue $\mu$, and the vertex subset $X=V(G-H)$ is called a star set for $\mu$ in $G$. The study of star complements and star sets provides a strong link between graph structure and linear algebra. In this paper, we study the regular graphs with $K_{t,s}\ (s\geq t\geq 2)$as a star complement for an eigenvalue$\mu$, especially, characterize the case of$t=3$completely, obtain some properties when$t=s$, and propose some problems for further study

Morphological growth performance and genetic parameters on Korean pine in Northeastern China

Korean pine (Pinus koraiensis) is an economically valuable species owing to its excellent timber quality and nuts useful for various purposes. But few studies have been made on growth performance, and aspects combining the genetic gain and classification method on phenotypic similarity in the selection process of superior families. Thus, the present study aimed at analyzing the genetic variation and highlight suitable morphological traits for family selection; establishing trait correlations and families' ordination based on similarities in phenotypic characters, and selecting elite families and suitable parent trees. Full-sib families from 28 crosses established in randomized complete block design from Naozhi orchard in Northeast China were used, and 11 morphological traits were investigated. Significant differences were observed among families for all traits. The traits coefficients of variation ranged from 6.07 to 56.25 % and from 0.029 to 15.213 % in phenotype and genotypic variation, respectively. A moderate level of inherited genetic control was observed (broad sense heritability H-2, varied from 0.155 to 0.438). Traits related to stem growth were highly positively correlated to each other whereas crown traits showed a weak correlation with stem traits (Pearson correlation r, ranged from -0.161 to 0.956). Based on multi-trait comprehensive analysis, we selected six elite families and six parents, which resulted in a genetic gain of 5.6 %, 16.9 %, and 36.4 % in tree height, diameter at breast height, and volume, respectively. These results make a theoretical basis for selecting excellent families and establish orchards of Korean pine from improved seeds

Downregulating Notch counteracts KrasG12D-induced ERK activation and oxidative phosphorylation in myeloproliferative neoplasm.

The Notch signaling pathway contributes to the pathogenesis of a wide spectrum of human cancers, including hematopoietic malignancies. Its functions are highly dependent on the specific cellular context. Gain-of-function NOTCH1 mutations are prevalent in human T-cell leukemia, while loss of Notch signaling is reported in myeloid leukemias. Here, we report a novel oncogenic function of Notch signaling in oncogenic Kras-induced myeloproliferative neoplasm (MPN). We find that downregulation of Notch signaling in hematopoietic cells via DNMAML expression or Pofut1 deletion significantly blocks MPN development in KrasG12D mice in a cell-autonomous manner. Further mechanistic studies indicate that inhibition of Notch signaling upregulates Dusp1, a dual phosphatase that inactivates p-ERK, and downregulates cytokine-evoked ERK activation in KrasG12D cells. Moreover, mitochondrial metabolism is greatly enhanced in KrasG12D cells but significantly reprogrammed by DNMAML close to that in control cells. Consequently, cell proliferation and expanded myeloid compartment in KrasG12D mice are significantly reduced. Consistent with these findings, combined inhibition of the MEK/ERK pathway and mitochondrial oxidative phosphorylation effectively inhibited the growth of human and mouse leukemia cells in vitro. Our study provides a strong rational to target both ERK signaling and aberrant metabolism in oncogenic Ras-driven myeloid leukemia

Endogenous IL-1 receptor antagonist restricts healthy and malignant myeloproliferation.

Here we explored the role of interleukin-1β (IL-1β) repressor cytokine, IL-1 receptor antagonist (IL-1rn), in both healthy and abnormal hematopoiesis. Low IL-1RN is frequent in acute myeloid leukemia (AML) patients and represents a prognostic marker of reduced survival. Treatments with IL-1RN and the IL-1β monoclonal antibody canakinumab reduce the expansion of leukemic cells, including CD34+ progenitors, in AML xenografts. In vivo deletion of IL-1rn induces hematopoietic stem cell (HSC) differentiation into the myeloid lineage and hampers B cell development via transcriptional activation of myeloid differentiation pathways dependent on NFκB. Low IL-1rn is present in an experimental model of pre-leukemic myelopoiesis, and IL-1rn deletion promotes myeloproliferation, which relies on the bone marrow hematopoietic and stromal compartments. Conversely, IL-1rn protects against pre-leukemic myelopoiesis. Our data reveal that HSC differentiation is controlled by balanced IL-1β/IL-1rn levels under steady-state, and that loss of repression of IL-1β signaling may underlie pre-leukemic lesion and AML progression.We thank K. Tasken, J. Saarela and the NCMM at the University of Oslo (UiO), S. Kanse (UiO) and B. Smedsrød (UiT), for access to facilities. We acknowledge Center for Medical Genetics and Molecular Medicine, Haukeland University Hospital (Bergen, Norway) and R. Hovland for karyotyping, FISH, translocation and DNA analyses of AML and MDS patients included in this study, and Department of Pathology, Oslo University Hospital (Oslo, Norway) and S. Spetalen for deep sequencing. L.M. Gonzalez, L.T. Eliassen, X. Zhang, M. Ristic and other members of L. Arranz group, O.P. Rekvig, R. Doohan, L.D. Håland, M.I. Olsen, A. Urbanucci, J. Landskron, K.B. Larsen, R.A. Lyså and UiT Advanced Microscopy Core Facility, UiO and UiT Comparative Medicine Units, for assistance. P. Garcia and S. Mendez-Ferrer for providing NRASG12D and Nes-gfp mice, respectively. P. Garcia and L. Kurian for careful reading of the manuscript. E. Tenstad (Science Shaped) for artwork in schematics. We would also like to thank the AML and MDS patients, and healthy volunteers, who donated biological samples. Our work is supported by a joint meeting grant of the Northern Norway Regional Health Authority, the University Hospital of Northern Norway (UNN) and UiT (Strategisk-HN06-14), Young Research Talent grants from the Research Council of Norway, (Stem Cell Program, 247596; FRIPRO Program, 250901), and grants from the Norwegian Cancer Society (6765150), the Northern Norway Regional Health Authority (HNF1338-17), and the Aakre-Stiftelsen Foundation (2016/9050) to L.A. Vav-Cre NRASG12D experiments were supported by NIH grant R01CA152108 to J.Z.S

Endogenous IL-1 receptor antagonist restricts healthy and malignant myeloproliferation

Here we explored the role of interleukin-1β (IL-1β) repressor cytokine, IL-1 receptor antagonist (IL-1rn), in both healthy and abnormal hematopoiesis. Low IL-1RN is frequent in acute myeloid leukemia (AML) patients and represents a prognostic marker of reduced survival. Treatments with IL-1RN and the IL-1β monoclonal antibody canakinumab reduce the expansion of leukemic cells, including CD34+ progenitors, in AML xenografts. In vivo deletion of IL-1rn induces hematopoietic stem cell (HSC) differentiation into the myeloid lineage and hampers B cell development via transcriptional activation of myeloid differentiation pathways dependent on NFκB. Low IL-1rn is present in an experimental model of pre-leukemic myelopoiesis, and IL-1rn deletion promotes myeloproliferation, which relies on the bone marrow hematopoietic and stromal compartments. Conversely, IL-1rn protects against pre-leukemic myelopoiesis. Our data reveal that HSC differentiation is controlled by balanced IL-1β/IL-1rn levels under steady-state, and that loss of repression of IL-1β signaling may underlie pre-leukemic lesion and AML progression

Hepatitis B Virus X Protein Drives Multiple Cross-Talk Cascade Loops Involving NF-κB, 5-LOX, OPN and Capn4 to Promote Cell Migration

Hepatitis B virus X protein (HBx) plays an important role in the development of hepatocellular carcinoma (HCC). However, the mechanism remains unclear. Recently, we have reported that HBx promotes hepatoma cell migration through the upregulation of calpain small subunit 1 (Capn4). In addition, several reports have revealed that osteopontin (OPN) plays important roles in tumor cell migration. In this study, we investigated the signaling pathways involving the promotion of cell migration mediated by HBx. We report that HBx stimulates several factors in a network manner to promote hepatoma cell migration. We showed that HBx was able to upregulate the expression of osteopontin (OPN) through 5-lipoxygenase (5-LOX) in HepG2-X/H7402-X (stable HBx-transfected cells) cells. Furthermore, we identified that HBx could increase the expression of 5-LOX through nuclear factor-κB (NF-κB). We also found that OPN could upregulate Capn4 through NF-κB. Interestingly, we showed that Capn4 was able to upregulate OPN through NF-κB in a positive feedback manner, suggesting that the OPN and Capn4 proteins involving cell migration affect each other in a network through NF-κB. Importantly, NF-κB plays a crucial role in the regulation of 5-LOX, OPN and Capn4. Thus, we conclude that HBx drives multiple cross-talk cascade loops involving NF-κB, 5-LOX, OPN and Capn4 to promote cell migration. This finding provides new insight into the mechanism involving the promotion of cell migration by HBx

The maximum spectral radius of graphs of given size with forbidden subgraph

Let $G$ be a graph of size $m$ and $\rho(G)$ be the spectral radius of its adjacency matrix. A graph is said to be $F$-free if it does not contain a subgraph isomorphic to $F$. In this paper, we prove that if $G$ is a $K_{2,r+1}$-free non-star graph with $m\geq (4r+2)^2+1$, then $\rho(G)\leq \rho(S_m^1)$. Recently, Li, Sun and Wei \cite{li2022} showed that for any $\theta_{1,2,3}$-free graph of size $m\geq 8$, $\rho(G)\leq \frac{1+\sqrt{4m-3}}{2}$, with equality if and only if $G\cong S_{\frac{m+3}{2},2}$. However, this bound is not attainable when $m$ is even. We proved that if $G$ is $\theta_{1,2,3}$-free and $G\ncong S_{\frac{m+3}{2},2}$ with $m\geq 22$, then $\rho(G)\leq \rho_1$ if $m$ is even, with equality if and only if $G\cong F_{m,1}$, and $\rho(G)\leq \rho_2$ if $m$ is odd, with equality if and only if $G\cong F_{m,1}$, where $\rho_t$ is the largest root of $x^4-mx^2-(m-t-1)x+\frac{t}{2}\cdot (m-t-1)=0$ for $t=1,2$.Comment: 14 pages, 3 figure

Free-Standing and Heteroatoms-Doped Carbon Nanofiber Networks as a Binder-Free Flexible Electrode for High-Performance Supercapacitors

Flexible and heteroatoms-doped (N, O and P) activated carbon nanofiber networks (ACFNs) have been successfully prepared with a mixture of polyamic acid (PAA) and poly(diaryloxyphosphazene) (PDPP) as a solution through electrospinning, followed by a heat post-treatment. The resultant heteroatoms-doped ACFNs can be used as binder-free electrodes for high-performance flexible supercapacitors (SCs) due to lightweight, three-dimensional open-pore structure and good mechanical strength. Despite its surface area being lower than 130.6 m2·g−1, the heteroatoms-doped ACFNs exhibited a high heteroatoms (N, O and P) content of 17.9%, resulting in a highly specific capacitance of 182 F·g−1 at a current density of 1 A·g−1 in 6 M KOH electrolyte in a two-electrode cell and an excellent rate capability of 74.7% of its initial capacitance from 1 A·g−1 to 10 A·g−1 under the mass loading of 1.5 mg·cm−2. The electrical double-layer (EDL) capacitance and pseudocapacitance can be easily decoupled in the heteroatoms-doped mesoporous ACFNs. SCs device based on heteroatoms-doped ACFNs exhibited a high energy density of 6.3 W·h·kg−1 with a power density of 250 W·kg−1, as well as excellent cycling stability with 88% capacitance retention after 10,000 charge–discharge cycles. The excellent electrochemical performance was attributed to the mesoporous structure of ACFNs and pseudocapacitive heteroatoms