The star-structure connectivity and star-substructure connectivity of hypercubes and folded hypercubes

As a generalization of vertex connectivity, for connected graphs $G$ and $T$, the $T$-structure connectivity $\kappa(G, T)$ (resp. $T$-substructure connectivity $\kappa^{s}(G, T)$) of $G$ is the minimum cardinality of a set of subgraphs $F$ of $G$ that each is isomorphic to $T$ (resp. to a connected subgraph of $T$) so that $G-F$ is disconnected. For $n$-dimensional hypercube $Q_{n}$, Lin et al. [6] showed $\kappa(Q_{n},K_{1,1})=\kappa^{s}(Q_{n},K_{1,1})=n-1$ and $\kappa(Q_{n},K_{1,r})=\kappa^{s}(Q_{n},K_{1,r})=\lceil\frac{n}{2}\rceil$ for $2\leq r\leq 3$ and $n\geq 3$. Sabir et al. [11] obtained that $\kappa(Q_{n},K_{1,4})=\kappa^{s}(Q_{n},K_{1,4})=\lceil\frac{n}{2}\rceil$ for $n\geq 6$, and for $n$-dimensional folded hypercube $FQ_{n}$, $\kappa(FQ_{n},K_{1,1})=\kappa^{s}(FQ_{n},K_{1,1})=n$, $\kappa(FQ_{n},K_{1,r})=\kappa^{s}(FQ_{n},K_{1,r})=\lceil\frac{n+1}{2}\rceil$ with $2\leq r\leq 3$ and $n\geq 7$. They proposed an open problem of determining $K_{1,r}$-structure connectivity of $Q_n$ and $FQ_n$ for general $r$. In this paper, we obtain that for each integer $r\geq 2$, $\kappa(Q_{n};K_{1,r})=\kappa^{s}(Q_{n};K_{1,r})=\lceil\frac{n}{2}\rceil$ and $\kappa(FQ_{n};K_{1,r})=\kappa^{s}(FQ_{n};K_{1,r})= \lceil\frac{n+1}{2}\rceil$ for all integers $n$ larger than $r$ in quare scale. For $4\leq r\leq 6$, we separately confirm the above result holds for $Q_n$ in the remaining cases

The structure connectivity of Data Center Networks

Last decade, numerous giant data center networks are built to provide increasingly fashionable web applications. For two integers $m\geq 0$ and $n\geq 2$, the $m$-dimensional DCell network with $n$-port switches $D_{m,n}$ and $n$-dimensional BCDC network $B_{n}$ have been proposed. Connectivity is a basic parameter to measure fault-tolerance of networks. As generalizations of connectivity, structure (substructure) connectivity was recently proposed. Let $G$ and $H$ be two connected graphs. Let $\mathcal{F}$ be a set whose elements are subgraphs of $G$, and every member of $\mathcal{F}$ is isomorphic to $H$ (resp. a connected subgraph of $H$). Then $H$-structure connectivity $\kappa(G; H)$ (resp. $H$-substructure connectivity $\kappa^{s}(G; H)$) of $G$ is the size of a smallest set of $\mathcal{F}$ such that the rest of $G$ is disconnected or the singleton when removing $\mathcal{F}$. Then it is meaningful to calculate the structure connectivity of data center networks on some common structures, such as star $K_{1,t}$, path $P_k$, cycle $C_k$, complete graph $K_s$ and so on. In this paper, we obtain that $\kappa (D_{m,n}; K_{1,t})=\kappa^s (D_{m,n}; K_{1,t})=\lceil \frac{n-1}{1+t}\rceil+m$ for $1\leq t\leq m+n-2$ and $\kappa (D_{m,n}; K_s)= \lceil\frac{n-1}{s}\rceil+m$ for $3\leq s\leq n-1$ by analyzing the structural properties of $D_{m,n}$. We also compute $\kappa(B_n; H)$ and $\kappa^s(B_n; H)$ for $H\in \{K_{1,t}, P_{k}, C_{k}|1\leq t\leq 2n-3, 6\leq k\leq 2n-1 \}$ and $n\geq 5$ by using $g$-extra connectivity of $B_n$

Star Structure Connectivity of Folded hypercubes and Augmented cubes

The connectivity is an important parameter to evaluate the robustness of a network. As a generalization, structure connectivity and substructure connectivity of graphs were proposed. For connected graphs $G$ and $H$, the $H$-structure connectivity $\kappa(G; H)$ (resp. $H$-substructure connectivity $\kappa^{s}(G; H)$) of $G$ is the minimum cardinality of a set of subgraphs $F$ of $G$ that each is isomorphic to $H$ (resp. to a connected subgraph of $H$) so that $G-F$ is disconnected or the singleton. As popular variants of hypercubes, the $n$-dimensional folded hypercubes $FQ_{n}$ and augmented cubes $AQ_{n}$ are attractive interconnected network prototypes for multiple processor systems. In this paper, we obtain that $\kappa(FQ_{n};K_{1,m})=\kappa^{s}(FQ_{n};K_{1,m})=\lceil\frac{n+1}{2}\rceil$ for $2\leqslant m\leqslant n-1$, $n\geqslant 7$, and $\kappa(AQ_{n};K_{1,m})=\kappa^{s}(AQ_{n};K_{1,m})=\lceil\frac{n-1}{2}\rceil$ for $4\leqslant m\leqslant \frac{3n-15}{4}$

Panton-Valentine Leukocidin Does Play a Role in the Early Stage of Staphylococcus aureus Skin Infections: A Rabbit Model

Despite epidemiological data linking necrotizing skin infections with the production of Panton-Valentine leukocidin (PVL), the contribution of this toxin to the virulence of S. aureus has been highly discussed as a result of inconclusive results of in vivo studies. However, the majority of these results originate from experiments using mice, an animal species which neutrophils - the major target cells for PVL - are highly insensitive to the action of this leukocidin. In contrast, the rabbit neutrophils have been shown to be as sensitive to PVL action as human cells, making the rabbit a better experimental animal to explore the PVL role. In this study we examined whether PVL contributes to S. aureus pathogenicity by means of a rabbit skin infection model. The rabbits were injected intradermally with 108 cfu of either a PVL positive community-associated methicillin-resistant S. aureus isolate, its isogenic PVL knockout or a PVL complemented knockout strain, and the development of skin lesions was observed. While all strains induced skin infection, the wild type strain produced larger lesions and a higher degree of skin necrosis compared to the PVL knockout strain in the first week after the infection. The PVL expression in the rabbits was indirectly confirmed by a raise in the serum titer of anti-LukS-PV antibodies observed only in the rabbits infected with PVL positive strains. These results indicate that the rabbit model is more suitable for studying the role of PVL in staphylococcal diseases than other animal models. Further, they support the epidemiological link between PVL producing S. aureus strains and necrotizing skin infections

Higher incidence of perineal community acquired MRSA infections among toddlers

<p>Abstract</p> <p>Background</p> <p>A six-fold increase in pediatric MRSA infections, prompted us to examine the clinical profile of children with MRSA infections seen at Mercy Children's Hospital, Toledo, Ohio and to characterize the responsible strains.</p> <p>Methods</p> <p>Records were reviewed of pediatric patients who cultured positive for MRSA from June 1 to December 31, 2007. Strain typing by pulsed field gel electrophoresis (PFT) and DiversiLab, SCC<it>mec </it>typing, and PCR-based <it>lukSF-PV </it>gene (encodes Panton-Valentine leukocidin), arginine catabolic mobile element (ACME) and <it>cap</it>5 gene detection was performed.</p> <p>Results</p> <p>Chart review of 63 patients with MRSA infections revealed that 58(92%) were community acquired MRSA (CAMRSA). All CAMRSA were skin and soft tissue infections (SSTI). Twenty five (43%) patients were aged < 3 yrs, 19(33%) aged 4-12 and 14(24%) aged 13-18. Nineteen (76%) of those aged < 3 yrs had higher incidence of perineal infections compared to only 2(11%) of the 4-12 yrs and none of the 13-18 yrs of age. Infections in the extremities were more common in the older youth compared to the youngest children. Overall, there was a significant association between site of the infection and age group (Fisher's Exact p-value < 0.001). All CAMRSA were USA300 PFT, clindamycin susceptible, SCC<it>mec </it>type IVa and <it>lukSF-PV gene </it>positive. Nearly all contained ACME and about 80% were <it>cap</it>5 positive. Of the 58 USA300 strains by PFT, 55(95%) were also identified as USA300 via the automated repetitive sequence-based PCR method from DiversiLab.</p> <p>Conclusions</p> <p>CAMRSA SSTI of the perineum was significantly more common among toddlers and that of the extremities in older children. The infecting strains were all USA300 PFT. Further studies are needed to identify the unique virulence and colonization characteristics of USA300 strains in these infections.</p

MRSA in Conventional and Alternative Retail Pork Products

In order to examine the prevalence of Staphylococcus aureus on retail pork, three hundred ninety-five pork samples were collected from a total of 36 stores in Iowa, Minnesota, and New Jersey. S. aureus was isolated from 256 samples (64.8%, 95% confidence interval [CI] 59.9%–69.5%). S. aureus was isolated from 67.3% (202/300) of conventional pork samples and from 56.8% (54/95) of alternative pork samples (labeled “raised without antibiotics” or “raised without antibiotic growth promotants”). Two hundred and thirty samples (58.2%, 95% CI 53.2%–63.1%) were found to carry methicillin-sensitive S. aureus (MSSA). MSSA was isolated from 61.0% (183/300) of conventional samples and from 49.5% (47/95) of alternative samples. Twenty-six pork samples (6.6%, 95% CI 4.3%–9.5%) carried methicillin-resistant S. aureus (MRSA). No statistically significant differences were observed for the prevalence of S. aureus in general, or MSSA or MRSA specifically, when comparing pork products from conventionally raised swine and swine raised without antibiotics, a finding that contrasts with a prior study from the Netherlands examining both conventional and “biologic” meat products. In our study spa types associated with “livestock-associated” ST398 (t034, t011) were found in 26.9% of the MRSA isolates, while 46.2% were spa types t002 and t008—common human types of MRSA that also have been found in live swine. The study represents the largest sampling of raw meat products for MRSA contamination to date in the U.S. MRSA prevalence on pork products was higher than in previous U.S.-conducted studies, although similar to that in Canadian studies

Emodin Suppresses Migration and Invasion through the Modulation of CXCR4 Expression in an Orthotopic Model of Human Hepatocellular Carcinoma

10.1371/journal.pone.0057015PLoS ONE83

Solid Tumor-Targeted Infiltrating Cytotoxic T Lymphocytes Retained by a Superantigen Fusion Protein

Successful immune-mediated regression of solid tumors is difficult because of the small number of cytotoxic T lymphocytes (CTLs) that were traffic to the tumor site. Here, the targeting of tumor-specific infiltrating CTLs was dependent on a fusion protein consisting of human epidermal growth factor (EGF) and staphylococcal enterotoxin A (SEA) with the D227A mutation. EGF-SEA strongly restrained the growth of murine solid sarcoma 180 (S180) tumors (control versus EGF-SEA, mean tumor weight: 1.013 versus 0.197 g, difference  = 0.816 g). In mice treated with EGF-SEA, CD4+, CD8+ and SEA-reactive T lymphocytes were enriched around the EGFR expressing tumor cells. The EGF receptors were potentially phosphorylated by EGF-SEA stimulation and the fusion protein promoted T cells to release the tumoricidal cytokines interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α). Intratumoral CTLs secreted cytolytic pore-forming perforins and granzyme B proteins near the surface of carcinomas, causing the death of many tumor cells. We additionally show that labeled EGF-SEA was directly targeted to the tumor tissue after intravenous (i.v.) injection. The findings demonstrate that antibody-like EGF-SEA plays an important role in arresting CTLs in the solid tumor site and has therapeutic potential as a tumor-targeting agent

Staphylococcus aureus Panton-Valentine Leukocidin Is a Very Potent Cytotoxic Factor for Human Neutrophils

The role of the pore-forming Staphylococcus aureus toxin Panton-Valentine leukocidin (PVL) in severe necrotizing diseases is debated due to conflicting data from epidemiological studies of community-associated methicillin-resistant S. aureus (CA-MRSA) infections and various murine disease-models. In this study, we used neutrophils isolated from different species to evaluate the cytotoxic effect of PVL in comparison to other staphylococcal cytolytic components. Furthermore, to study the impact of PVL we expressed it heterologously in a non-virulent staphylococcal species and examined pvl-positive and pvl-negative clinical isolates as well as the strain USA300 and its pvl-negative mutant. We demonstrate that PVL induces rapid activation and cell death in human and rabbit neutrophils, but not in murine or simian cells. By contrast, the phenol-soluble modulins (PSMs), a newly identified group of cytolytic staphylococcal components, lack species-specificity. In general, after phagocytosis of bacteria different pvl-positive and pvl-negative staphylococcal strains, expressing a variety of other virulence factors (such as surface proteins), induced cell death in neutrophils, which is most likely associated with the physiological clearing function of these cells. However, the release of PVL by staphylococcal strains caused rapid and premature cell death, which is different from the physiological (and programmed) cell death of neutrophils following phagocytosis and degradation of virulent bacteria. Taken together, our results question the value of infection-models in mice and non-human primates to elucidate the impact of PVL. Our data clearly demonstrate that PVL acts differentially on neutrophils of various species and suggests that PVL has an important cytotoxic role in human neutrophils, which has major implications for the pathogenesis of CA-MRSA infections