Secondary infection with Streptococcus suis serotype 7 increases the virulence of highly pathogenic porcine reproductive and respiratory syndrome virus in pigs

<p>Abstract</p> <p>Background</p> <p>Porcine reproductive and respiratory syndrome virus (PRRSV) and <it>Streptococcus suis </it>are common pathogens in pigs. In samples collected during the porcine high fever syndrome (PHFS) outbreak in many parts of China, PRRSV and <it>S. suis </it>serotype 7 (SS7) have always been isolated together. To determine whether PRRSV-SS7 coinfection was the cause of the PHFS outbreak, we evaluated the pathogenicity of PRRSV and/or SS7 in a pig model of single and mixed infection.</p> <p>Results</p> <p>Respiratory disease, diarrhea, and anorexia were observed in all infected pigs. Signs of central nervous system (CNS) disease were observed in the highly pathogenic PRRSV (HP-PRRSV)-infected pigs (4/12) and the coinfected pigs (8/10); however, the symptoms of the coinfected pigs were clearly more severe than those of the HP-PRRSV-infected pigs. The mortality rate was significantly higher in the coinfected pigs (8/10) than in the HP-PRRSV- (2/12) and SS7-infected pigs (0/10). The deceased pigs of the coinfected group had symptoms typical of PHFS, such as high fever, anorexia, and red coloration of the ears and the body. The isolation rates of HP-PRRSV and SS7 were higher and the lesion severity was greater in the coinfected pigs than in monoinfected pigs.</p> <p>Conclusion</p> <p>HP-PRRSV infection increased susceptibility to SS7 infection, and coinfection of HP-PRRSV with SS7 significantly increased the pathogenicity of SS7 to pigs.</p

Phase field simulation for grain refinement in dendrite growth of A356 aluminum alloy

Although A356 aluminum alloy has poor ductility and strength, the refinement of the initial α-Al phase has shown promise in improving these properties. The impact of grain refinement mechanisms on the organization and morphology of A356 aluminum alloys has not been thoroughly investigated. In this paper, we constructed a phase field lattice-Boltzmann model to explore the influence of the refinement mechanism on the growth of α-Al dendrites during the non-isothermal solidification process of A356 aluminum alloy. The results demonstrated that the approach of alloying by adding elements, introducing forced convection, and increasing the degree of subcooling has proven to be effective in refining the dendrites of A356 aluminum alloy. The presence of Fe element further promotes the thinning of α-Al dendrites, and this effect is also found after melting ultrasonic treatment at a lower initial casting temperature. These findings are expected to provide theoretical support for effectively improving the hardness, ductility, and overall performance of Al-based alloys

Deoxynivalenol Induces Inflammation in IPEC-J2 Cells by Activating P38 Mapk And Erk1/2

Fusarium-derived mycotoxin deoxynivalenol (DON) usually induces diarrhea, vomiting and gastrointestinal inflammation. We studied the cytotoxic effect of DON on porcine small intestinal epithelium using the intestinal porcine epithelial cell line IPEC-J2. We screened out differentially expressed genes (DEGs) using RNA-seq and identified 320 upregulated genes and 160 downregulated genes. The enrichment pathways of these DEGs focused on immune-related pathways. DON induced proinflammatory gene expression, including cytokines, chemokines and other inflammation-related genes. DON increased IL1A, IL6 and TNF-&alpha; release and DON activated the phosphorylation of extracellular signal-regulated kinase-1 and-2 (ERK1/2), JUN N-terminal kinase (JNK) and p38 MAPK. A p38 inhibitor attenuated DON-induced IL6, TNF-&alpha;, CXCL2, CXCL8, IL12A, IL1A, CCL20, CCL4 and IL15 production, while an ERK1/2 inhibitor had only a small inhibitory effect on IL15 and IL6. An inhibitor of p38 MAPK decreased the release of IL1A, IL6 and TNF-&alpha; and an inhibitor of ERK1/2 partly attenuated protein levels of IL6. These data demonstrate that DON induces proinflammatory factor production in IPEC-J2 cells by activating p38 and ERK1/2

Automatic Illumination Control Method for Indoor Luminaires Based on Multichromatic Quantum Dot Light-Emitting Diodes

Energy saving and visual comfort are two main considerations in designing of automatic illumination control systems. However, energy-saving-oriented illumination control always causes optical spectra drifting in light-conversion-material-based white light-emitting diodes (WLEDs), which are conventionally used as artificial luminaires in indoor areas. In this study, we propose a method for InP quantum dot (QD)-based WLEDs to minimize optical energy consumption by considering the influence caused by the outdoor environment and neighboring WLED units. Factors of (a) dimensions of room window and WLED matrix, (b) distance between WLED units, lighting height, species of InP QDs, and (c) user distribution are taken into consideration in calculation. Parameters of correlated color temperature (CCT) and color rendering index (Ra) of the WLED matrix are optimized according to the lighting environment to improve user visual comfort level. By dynamically controlling the light ingredients and optical power of WLEDs, we optimize the received illuminance distribution of table tops, improve the lighting homogeneity of all users, and guarantee the lowest energy consumption of the WLED matrix. The proposed approach can be flexibly applied in large-scale WLED intelligent controlling systems for industrial workshops and office buildings

Glucose-Dependent Insulinotropic Polypeptide and Substance P Mediate Emetic Response Induction by Masked Trichothecene Deoxynivalenol-3-Glucoside through Ca2+ Signaling

Deoxynivalenol (DON), the most naturally-occurring trichothecenes, may affect animal and human health by causing vomiting as a hallmark of food poisoning. Deoxynivalenol-3-glucoside (D3G) usually co-occurs with DON as its glucosylated form and is another emerging food safety issue in recent years. However, the toxicity of D3G is not fully understood compared to DON, especially in emetic potency. The goals of this research were to (1) compare emetic effects to D3G by oral and intraperitoneal (IP) routes and relate emetic effects to brain-gut peptides glucose-dependent insulinotropic polypeptide (GIP) and substance P (SP) in mink; (2) determine the roles of calcium-sensing receptor (CaSR) and transient receptor potential (TRP) channel in D3G&rsquo;s emetic effect. Both oral and IP exposure to D3G elicited marked emetic events. This emetic response corresponded to an elevation of GIP and SP. Blocking the GIP receptor (GIPR) diminished emetic response induction by GIP and D3G. The neurokinin 1 receptor (NK-1R) inhibitor Emend&reg; restrained the induction of emesis by SP and D3G. Importantly, CaSR antagonist NPS-2143 or TRP channel antagonist ruthenium red dose-dependently inhibited both D3G-induced emesis and brain-gut peptides GIP and SP release; cotreatment with both antagonists additively suppressed both emetic and brain-gut peptide responses to D3G. To summarize, our findings demonstrate that activation of CaSR and TRP channels contributes to D3G-induced emesis by mediating brain-gut peptide exocytosis in mink

Architecture of the photosynthetic complex from a green sulfur bacterium

The photosynthetic apparatus of green sulfur bacteria (GSB) contains a peripheral antenna chlorosome, light-harvesting Fenna-Matthews-Olson proteins (FMO), and a reaction center (GsbRC). We used cryo-electron microscopy to determine a 2.7-angstrom structure of the FMO-GsbRC supercomplex from Chlorobaculum tepidum. The GsbRC binds considerably fewer (bacterio) chlorophylls [(B)Chls] than other known type I RCs do, and the organization of (B)Chls is similar to that in photosystem II. Two BChl layers in GsbRC are not connected by Chls, as seen in other RCs, but associate with two carotenoid derivatives. Relatively long distances of 22 to 33 angstroms were observed between BChls of FMO and GsbRC, consistent with the inefficient energy transfer between these entities. The structure contains common features of both type I and type II RCs and provides insight into the evolution of photosynthetic RCs

A unique photosystem I reaction center from a chlorophyll d-containing cyanobacterium Acaryochloris marina

Photosystem I (PSI) is a large protein supercomplex that catalyzes the light-dependent oxidation of plastocyanin (or cytochrome c(6)) and the reduction of ferredoxin. This catalytic reaction is realized by a transmembrane electron transfer chain consisting of primary electron donor (a special chlorophyll (Chl) pair) and electron acceptors A(0), A(1), and three Fe4S4 clusters, F-X, F-A, and F-B. Here we report the PSI structure from a Chl d-dominated cyanobacterium Acaryochloris marina at 3.3 angstrom resolution obtained by single-particle cryo-electron microscopy. The A. marina PSI exists as a trimer with three identical monomers. Surprisingly, the structure reveals a unique composition of electron transfer chain in which the primary electron acceptor A(0) is composed of two pheophytin a rather than Chl a found in any other well-known PSI structures. A novel subunit Psa27 is observed in the A. marina PSI structure. In addition, 77 Chls, 13 alpha-carotenes, two phylloquinones, three Fe-S clusters, two phosphatidyl glycerols, and one monogalactosyl-diglyceride were identified in each PSI monomer. Our results provide a structural basis for deciphering the mechanism of photosynthesis in a PSI complex with Chl d as the dominating pigments and absorbing far-red light