Identification by PCR signature-tagged mutagenesis of attenuated Salmonella Pullorum mutants and corresponding genes in a chicken embryo model

A key feature of the fowl-specific pathogen Salmonella Pullorum is its vertical transmission to progeny via the egg. In this study, PCR signature-tagged mutagenesis identified nine genes of a strain of S. Pullorum that contributed to survival in the chicken embryo during incubation. The genes were involved in invasion, cell division, metabolism and bacterial defence. The competition index in vivo and in vitro together with a virulence evaluation for chicken embryos of all nine mutant strains confirmed their attenuation

Skin Mast Cells Contribute to Sporothrix schenckii Infection

Background: Sporothrix schenckii (S. schenckii), a dimorphic fungus, causes sporotrichosis. Mast cells (MCs) have been described to be involved in skin fungal infections. The role of MCs in cutaneous sporotrichosis remains largely unknown. Objectives: To characterize the role and relevance of MCs in cutaneous sporotrichosis. Methods: We analyzed cutaneous sporotrichosis in wild-type (WT) mice and two different MC-deficient strains. In vitro, MCs were assessed for S. schenckii-induced cytokine production and degranulation after incubation with S. schenckii. We also explored the role of MCs in human cutaneous sporotrichosis. Results: WT mice developed markedly larger skin lesions than MC-deficient mice (> 1.5 fold) after infection with S. schenckii, with significantly increased fungal burden. S. schenckii induced the release of tumor necrosis factor alpha (TNF), interleukin (IL)-6, IL-10, and IL-1β by MCs, but not degranulation. S. schenckii induced larger skin lesions and higher release of IL-6 and TNF by MCs as compared to the less virulent S. albicans. In patients with sporotrichosis, TNF and IL-6 were increased in skin lesions, and markedly elevated levels in the serum were linked to disease activity. Conclusions: These findings suggest that cutaneous MCs contribute to skin sporotrichosis by releasing cytokines such as TNF and IL-6

Information-Theoretic Limits of Bistatic Integrated Sensing and Communication

The bistatic integrated sensing and communication (ISAC) system model avoids the strong self-interference in a monostatic ISAC system by employing a pair of physically separated sensing transceiver and maintaining the merit of co-designing radar sensing and communications on shared spectrum and hardware. Inspired by the appealing benefits of bistatic radar, we study bistatic ISAC, where a transmitter sends a message to a communication receiver and a sensing receiver at another location carries out a decoding-and-estimation(DnE) operation to obtain the state of the communication receiver. In this paper, both communication and sensing channels are modelled as state-dependent memoryless channels with independent and identically distributed time-varying state sequences. We consider a rate of reliable communication for the message at the communication receiver as communication metric. The objective of this model is to characterize the capacity-distortion region, i.e., the set of all the achievable rate while simultaneously allowing the sensing receiver to sense the state sequence with a given distortion threshold. In terms of the decoding degree on this message at the sensing receiver, we propose three achievable DnE strategies, the blind estimation, the partial-decoding-based estimation, and the full-decoding-based estimation, respectively. Based on the three strategies, we derive the three achievable rate-distortion regions. In addition, under the constraint of the degraded broadcast channel, i.e., the communication receiver is statistically stronger than the sensing receiver, and the partial-decoding-based estimation, we characterize the capacity region. Examples in both non-degraded and degraded cases are provided to compare the achievable rate-distortion regions under three DnE strategies and demonstrate the advantages of ISAC over independent communication and sensing.Comment: 40 pages, 7 figure

Roles of the spiA gene from Salmonella enteritidis in biofilm formation and virulence

Salmonella enteritidis has emerged as one of the most important food-borne pathogens for humans, and the formation of biofilms by this species may improve its resistance to disadvantageous conditions. The spiA gene of Salmonella typhimurium is essential for its virulence in host cells. However, the roles of the spiA gene in biofilm formation and virulence of S. enteritidis remain unclear. In this study we constructed a spiA gene mutant with a suicide plasmid. Phenotypic and biological analysis revealed that the mutant was similar to the wild-type strain in growth rate, morphology, and adherence to and invasion of epithelial cells. However, the mutant showed reduced biofilm formation in a quantitative microtitre assay and by scanning electron microscopy, and significantly decreased curli production and intracellular proliferation of macrophages during the biofilm phase. In addition, the spiA mutant was attenuated in a mouse model in both the exponential growth and biofilm phases. These data indicate that the spiA gene is involved in both biofilm formation and virulence of S. enteritidis

Significantly enhanced creep resistance of low volume fraction in-situ TiBw/Ti6Al4V composites by architectured network reinforcements

We present a new class of TiBw/Ti6Al4V composites with a network reinforcement architecture that exhibits a significant creep resistance compared to monolithic Ti6Al4V alloys. Creep tests performed at temperatures between 773 K and 923 K and stress range of 100 MPa-300 MPa indicate both a significant improvement of the composites creep resistance due to the network architecture made by the TiB whiskers (TiBw), and a decrease of the steady-state creep rates by augmenting the local volume fractions of TiBw in the network region. The deformation behavior is driven by a diffusion-controlled dislocation climb process. Moreover, the activation energies of these composites are significantly higher than that of Ti6Al4V alloys, indicating a higher creep resistance. The increase of the activation energy can be attributed to the TiBw architecture that severely impedes the movements of dislocation and grain boundary sliding and provides a tailoring of the stress transfer. These micromechanical mechanisms lead to a remarkable improvement of the creep resistance of these networked TiBw/Ti6Al4V composites featuring the special networked architecture