Plasma n-3 and n-6 fatty acids and inflammatory markers in Chinese vegetarians

Background: Polyunsaturated fatty acid (PUFA) intake favorably affects chronic inflammatory-related diseases such as cardiovascular disease; however, the relationship between the PUFA and inflammatory factors in the healthy vegetarians were not clear. We aimed to investigate the plasma fatty acids status, and its association with plasma inflammatory factors in Chinese vegetarians and omnivores. Methods: A total of 89 male vegetarians and 106 male omnivores were participated the study. Plasma concentrations of inflammatory factors were detected by ELISA, and as standard methods fatty acids were extracted and determined by chromatography. Results: Compared with omnivores, vegetarians have significant higher interleukin-6 (IL-6), plasma n-6 PUFA, n-6/n-3, and 18:3n-3; while they have significant lower leukotriene B4 (LTB4), cyclo-oxygenase-2 (COX2) and prostaglandin E2 (PGE2), 20:5n-3, 22:5n-3, 22:6n-3, and n-3 PUFA. In vegetarians, plasma 20:4n-6 was significant positively related to TNF-α. LTB4 was significantly positively related to plasma 22:6n-3, and negatively associated with n-6 PUFA. Conclusion: Vegetarians have higher plasma n-6 PUFA and IL-6, but lower LTB4, n-3 PUFA, 22:6n-3, COX2 and PGE2 levels. It would seem appropriate for vegetarians to increase their dietary n-3 PUFA, while reduce dietary n-6 PUFA and thus reduce the risk of chronic inflammatory-related diseases

The Role of Toll-Like Receptor 9 in Chronic Stress-Induced Apoptosis in Macrophage

Emerging evidence implied that chronic stress has been exerting detrimental impact on immune system functions in both humans and animals. Toll-like receptors (TLRs) have been shown to play an essential role in modulating immune responses and cell survival.We have recently shown that TLR9 deficiency protects against lymphocyte apoptosis induced by chronic stress. However, the exact role of TLR9 in stress-mediated change of macrophage function remains unclear. The results of the current study showed that when BALB/c mice were treated with restraint stress (12 h daily for 2 days), the number of macrophages recruited to the peritoneal cavity was obviously increased. Results also demonstrated that the sustained effects of stress elevated cytokine IL-1β, TNF-α and IL-10 production yet diminished IFN-γ production from macrophage, which led to apoptotic cell death. However, TLR9 deficiency prevented the chronic stress-mediated accumulation of macrophages. In addition, knocking out TLR9 significantly abolished the chronic stress-induced imbalance of cytokine levels and apoptosis in macrophage. TLR9 deficiency was also found to reverse elevation of plasma IL-1β, IL-10 and IL-17 levels and decrease of plasma IFN-γ level under the condition of chronic stress. These results indicated that TLR9-mediated macrophage responses were required for chronic stress-induced immunosuppression. Further exploration showed that TLR9 deficiency prevented the increment of p38 MAPK phosphorylation and reduction of Akt/Gsk-3β phosphorylation; TLR9 deficiency also attenuated the release of mitochondrial cytochrome c into cytoplasm, caused upregulation of Bcl-2/Bax protein ratio, downregulation of cleavage of caspase-3 and PARP, as well as decreased TUNEL-positive cells in macrophage of stressed mice. Collectively, our studies demonstrated that deficiency of TLR9 maintained macrophage function by modulating macrophage accumulation and attenuating macrophage apoptosis, thus preventing immunosuppression in restraint-stressed mice

Mitochondrial protein dysfunction in pathogenesis of neurological diseases

Mitochondria are essential organelles for neuronal function and cell survival. Besides the well-known bioenergetics, additional mitochondrial roles in calcium signaling, lipid biogenesis, regulation of reactive oxygen species, and apoptosis are pivotal in diverse cellular processes. The mitochondrial proteome encompasses about 1,500 proteins encoded by both the nuclear DNA and the maternally inherited mitochondrial DNA. Mutations in the nuclear or mitochondrial genome, or combinations of both, can result in mitochondrial protein deficiencies and mitochondrial malfunction. Therefore, mitochondrial quality control by proteins involved in various surveillance mechanisms is critical for neuronal integrity and viability. Abnormal proteins involved in mitochondrial bioenergetics, dynamics, mitophagy, import machinery, ion channels, and mitochondrial DNA maintenance have been linked to the pathogenesis of a number of neurological diseases. The goal of this review is to give an overview of these pathways and to summarize the interconnections between mitochondrial protein dysfunction and neurological diseases.Peer reviewe

Genome plasticity of Vibrio parahaemolyticus: microevolution of the 'pandemic group'

<p>Abstract</p> <p>Background</p> <p>Outbreak of <it>V. parahaemolyticus </it>infections occurred since 1996 was linked to a proposed clonal complex, the pandemic group. The whole genome sequence provides an unprecedented opportunity for dissecting genome plasticity and phylogeny of the populations of <it>V. parahaemolyticus</it>. In the present work, a whole-genome cDNA microarray was constructed to compare the genomic contents of a collection of 174 strains of <it>V. parahaemolyticus</it>.</p> <p>Results</p> <p>Genes that present variably in the genome accounted for about 22% of the whole gene pool on the genome. The phylogenetic analysis of microarray data generated a minimum spanning tree that depicted the phylogenetic structure of the 174 strains. Strains were assigned into five complexes (C1 to C5), and those in each complex were related genetically and phylogenetically. C3 and C4 represented highly virulent clinical clones. C2 and C3 constituted two different clonal complexes 'old-O3:K6 clone' and 'pandemic clone', respectively. C3 included all the 39 pandemic strains tested (<it>trh</it>^-, <it>tdh</it>⁺and GS-PCR⁺), while C2 contained 12 pre-1996 'old' O3:K6 strains (<it>trh</it>⁺, <it>tdh</it>^-and GS-PCR^-) tested herein. The pandemic clone (post-1996 'new' O3:K6 and its derivates O4:K68, O1:K25, O1:KUT and O6:K18) might be emerged from the old-O3:K6 clone, which was promoted by acquisition of <it>toxRS</it>/new sequence and genomic islands. A phylogenetic intermediate O3:K6 clade (<it>trh</it>^-, <it>tdh</it>^-and GS-PCR⁺) was identified between the pandemic and old-O3:K6 clones.</p> <p>Conclusion</p> <p>A comprehensive overview of genomic contents in a large collection of global isolates from the microarray-based comparative genomic hybridization data enabled us to construct a phylogenetic structure of <it>V. parahaemolyticus </it>and an evolutionary history of the pandemic group (clone) of this pathogen.</p

An Improved Graph Drawing Algorithm for Email Networks

This paper addresses the graph drawing problem for email networks. First, the graph drawing problem is formulated as a minimization problem. Then, a genetic algorithm based graph drawing method is proposed by solving the minimization problem. By taking into account the small-world property of the email-networks, the proposed method improved the force-directed graph drawing algorithm to draw the graph more intuitively and aesthetically. It also speeds up the graph drawing algorithm by ignoring repulsive force far away from the vertex, and prevents the nearly disconnected graph from being pushed to the border. Moreover, the key cliques of the email networks are placed in the central of the layout. Experiment tests show that the proposed method has better performance in satisfying the aesthetic criterions and time consumption

Gas foaming of electrospun poly(L-lactide-co-caprolactone)/silk fibroin nanofiber scaffolds to promote cellular infiltration and tissue regeneration

Electrospun nanofibers emulate extracellular matrix (ECM) morphology and architecture; however, small pore size and tightly-packed fibers impede their translation in tissue engineering. Here we exploited in situ gas foaming to afford three-dimensional (3D) poly(L-lactide-co-ε-caprolactone)/silk fibroin (PLCL/SF) scaffolds, which exhibited nanotopographic cues and a multilayered structure. The addition of SF improved the hydro philicity and biocompatibility of 3D PLCL scaffolds. Three-dimensional scaffolds exhibited larger pore size (38.75 ± 9.78 μm2 ) and high porosity (87.1% ± 1.5%) than that of their 2D counterparts. 3D scaffolds also improved the deposition of ECM components and neo-vessel regeneration as well as exhibited more numbers of CD163+/ CCR7+ cells after 2 weeks implantation in a subcutaneous model. Collectively, 3D PLCL/SF scaffolds have broad implications for regenerative medicine and tissue engineering applications.info:eu-repo/semantics/publishedVersio

Catalytic Ozone Oxidation of Petrochemical Secondary Effluent: Mechanism, Application and Future Development

Petrochemical secondary effluent contains toxic and refractory organic compounds, which are difficult to be further treated by traditional biological process. In China, most of the advanced treatment units have been built recently by catalytic ozone oxidation process to achieve the high-quality effluent. In this chapter, the mechanism and reaction process of catalytic ozone oxidation of petrochemical secondary effluent will be introduced in detail. With the operation of the catalytic ozone oxidation tank, a series of problems which are not taken into account at the beginning of the design have arisen. The chapter will talk about the problems concerning the biological flocs, colloidal macromolecule organic compounds, ozone mass transfer, and catalysts based on practical applications. In the last part of the chapter, the development trends of catalytic ozone oxidation of petrochemical secondary effluent will also be discussed

Transcriptome and functional analysis revealed the intervention of brassinosteroid in regulation of cold induced early flowering in tobacco

Cold environmental conditions may often lead to the early flowering of plants, and the mechanism by cold-induced flowering remains poorly understood. Microscopy analysis in this study demonstrated that cold conditioning led to early flower bud differentiation in two tobacco strains and an Agilent Tobacco Gene Expression microarray was adapted for transcriptomic analysis on the stem tips of cold treated tobacco to gain insight into the molecular process underlying flowering in tobacco. The transcriptomic analysis showed that cold treatment of two flue-cured tobacco varieties (Xingyan 1 and YunYan 85) yielded 4176 and 5773 genes that were differentially expressed, respectively, with 2623 being commonly detected. Functional distribution revealed that the differentially expressed genes (DEGs) were mainly enriched in protein metabolism, RNA, stress, transport, and secondary metabolism. Genes involved in secondary metabolism, cell wall, and redox were nearly all up-regulated in response to the cold conditioning. Further analysis demonstrated that the central genes related to brassinosteroid biosynthetic pathway, circadian system, and flowering pathway were significantly enhanced in the cold treated tobacco. Phytochemical measurement and qRT-PCR revealed an increased accumulation of brassinolide and a decreased expression of the flowering locus c gene. Furthermore, we found that overexpression of NtBRI1 could induce early flowering in tobacco under normal condition. And low-temperature-induced early flowering in NtBRI1 overexpression plants were similar to that of normal condition. Consistently, low-temperature-induced early flowering is partially suppressed in NtBRI1 mutant. Together, the results suggest that cold could induce early flowering of tobacco by activating brassinosteroid signaling

Exome sequencing revealed PDE11A as a novel candidate gene for early-onset Alzheimer\u27s disease

To identify novel risk genes and better understand the molecular pathway underlying Alzheimer\u27s disease (AD), whole-exome sequencing was performed in 215 early-onset AD (EOAD) patients and 255 unrelated healthy controls of Han Chinese ethnicity. Subsequent validation, computational annotation and in vitro functional studies were performed to evaluate the role of candidate variants in EOAD. We identified two rare missense variants in the phosphodiesterase 11A (PDE11A) gene in individuals with EOAD. Both variants are located in evolutionarily highly conserved amino acids, are predicted to alter the protein conformation and are classified as pathogenic. Furthermore, we found significantly decreased protein levels of PDE11A in brain samples of AD patients. Expression of PDE11A variants and knockdown experiments with specific short hairpin RNA (shRNA) for PDE11A both resulted in an increase of AD-associated Tau hyperphosphorylation at multiple epitopes in vitro. PDE11A variants or PDE11A shRNA also caused increased cyclic adenosine monophosphate (cAMP) levels, protein kinase A (PKA) activation and cAMP response element-binding protein phosphorylation. In addition, pretreatment with a PKA inhibitor (H89) suppressed PDE11A variant-induced Tau phosphorylation formation. This study offers insight into the involvement of Tau phosphorylation via the cAMP/PKA pathway in EOAD pathogenesis and provides a potential new target for intervention