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Metabolomics provides an unprecedented window on diverse plant secondary metabolites that represent a potentially critical niche dimension in tropical forests underlying co-existence. Here, we used untargeted metabolomics to evaluate the chemical composition of 358 tree species and its relationship to phylogeny and variation in light environment, soil nutrients, and insect-herbivore leaf damage in a tropical rain forest plot. We found that tree species that co-occur locally are less chemically similar than random, and that local chemical dispersion and metabolite diversity reduce herbivory, especially that of specialist insect herbivores. Our results suggest that plant secondary metabolites have the potential to mediate plant-herbivore interactions in a manner consistent with diversity maintenance at the community scale.

Background and Aims Artemisia is a mega-diverse genus consisting of ~400 species. Despite its medicinal importance and ecological significance, a well-resolved phylogeny for global Artemisia, a natural generic delimitation and infrageneric taxonomy remain missing, owing to the obstructions from limited taxon sampling and insufficient information on DNA markers. Its morphological characters, such as capitulum, life form and leaf, show marked variations and are widely used in its infrageneric taxonomy. However, their evolution within Artemisia is poorly understood. Here, we aimed to reconstruct a well-resolved phylogeny for global Artemisia via a phylogenomic approach, to infer the evolutionary patterns of its key morphological characters and to update its circumscription and infrageneric taxonomy. Methods We sampled 228 species (258 samples) of Artemisia and its allies from both fresh and herbarium collections, covering all the subgenera and its main geographical areas, and conducted a phylogenomic analysis based on nuclear single nucleotide polymorphisms (SNPs) obtained from genome skimming data. Based on the phylogenetic framework, we inferred the possible evolutionary patterns of six key morphological characters widely used in its previous taxonomy. Key Results The genus Kaschgaria was revealed to be nested in Artemisia with strong support. A well-resolved phylogeny of Artemisia consisting of eight highly supported clades was recovered, two of which were identified for the first time. Most of the previously recognized subgenera were not supported as monophyletic. Evolutionary inferences based on the six morphological characters showed that different states of these characters originated independently more than once. Conclusions The circumscription of Artemisia is enlarged to include the genus Kaschgaria. The morphological characters traditionally used for the infrageneric taxonomy of Artemisia do not match the new phylogenetic tree. They experienced a more complex evolutionary history than previously thought. We propose a revised infrageneric taxonomy of the newly circumscribed Artemisia, with eight recognized subgenera to accommodate the new results., This work was supported by the National Natural Science Foundation of China (grant nos. 31870179, 31570204, 31270237 and J1310002), the International Partnership Program (grant no. 151853KYSB20190027), Sino-Africa Joint Research Center (grant no. SAJC201614), Key technology projects of Jiangxi Province's major scientific and technological research and development project (grant no. 20223AAF01007), Survey of Wildlife Resources in Key Areas of Tibet (grant no. ZL202203601) and National Plant Specimen Resource Center (grant no. E0117G1001) of the Chinese Academy of Sciences, Key Project at Central Government Level: The Ability Establishment of Sustainable Use of Valuable Chinese Medicine Resources (grant no. 2060302) and Project of the Central Siberian Botanical Garden of the Siberian Branch of the Russian Academy of Sciences (grant no. AAAA-A21-121011290024-5)., INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION Conclusions SUPPLEMENTARY DATA FUNDING ACKNOWLEDGEMENTS CONFLICT OF INTEREST LITERATURE CITED Supplementary data

As a newly emerging pathogen, Candida auris has spread rapidly and caused a serious invasive infection. Candida auris often appeared high resistance to classical antifungal drugs. Drug combination therapy is emerging as an effective and well-established strategy to relieve drug resistance problems. The objective of present work was to examine the activity of fluconazole in combination with chlorhexidine acetate against Candida auris isolates.Antiplanktonic activity was studied using the EUCAST methodology and growth curve assay. Antibiofilm effectiveness was determined by the crystal violet method, checkerboard microdilution assay, scanning electron microscopy, and confocal laser scanning microscopy.The results indicated that the 80% minimal inhibitory concentrations for fluconazole alone against Candida auris were 2-32 mg/L and for chlorhexidine acetate were 2-8 mg/L. The combination of fluconazole with chlorhexidine acetate exhibited synergism with the growth curve assay. In addition, the checkerboard microdilution assay presented that fluconazole was strongly synergistic with chlorhexidine acetate (sFICI0.1875) in inhibiting the growth of Candida auris biofilms. The scanning electron microscopy and confocal laser scanning microscopy further exhibited the alteration of morphology of the cells and architecture of the biofilms.The combination therapy of fluconazole and chlorhexidine acetate provides a new potential strategy for the treatment of clinical Candida auris infection.

MicroRNA‐122 (miR‐122) is known to be up‐regulated by inflammation to exert a variety of biological functions in hepatocellular carcinoma (HCC)‐derived human cell lines. Vitamin D receptor (VDR) is reported to regulate excessive oral keratinocytes apoptosis which compromises oral epithelial barrier in oral lichen planus (OLP). Although many studies have suggested that miR‐122 is capable of regulating cell apoptosis, its effects on the development of OLP and VDR expression are still unclear. Herein, we demonstrate that miR‐122 expression is increased in the epithelial layer of OLP. Mechanically, transcription factor nuclear factor‐κB (NF‐κB) selectively binds with κB element in the promoter of miR‐122 to accelerate gene transcription. The up‐regulation of miR‐122 induces cell apoptosis in human oral keratinocytes (HOKs) by targeting VDR mRNA. In VDR knockout oral keratinocytes, miR‐122 fails to improve caspase 3 activity and cleaved caspase 3 and poly(ADP‐ribose) polymerase (PARP) levels. Moreover, VDR overexpression is able to reverse lipopolysaccharide (LPS)‐ or activated CD4+ T cell–induced miR‐122 up‐regulation and ameliorate miR‐122‐stimulated caspase 3 activity. Collectively, our results suggest that miR‐122 promotes oral keratinocytes apoptosis in OLP through decreasing VDR expression.

Stimulator of interferon genes (STING) is reported to exert vital functions in inflammatory responses and autoimmune diseases. Nevertheless, the status and roles of STING in oral lichen planus (OLP) remain elusive. Here, we state that STING and its downstream cytokine interferon-β (IFNβ) expression is boosted in the oral keratinocytes from patients suffering OLP in comparison with those from healthy participants. Mechanistically, transcription factor GATA-binding protein 1 (GATA1) which is highly increased in diseased samples specifically interacts with its element in the promoter of STING to enhance STING transcripts. 1,25(OH)

Abstract: Mesenchymal stem cells derived from postnatal orofacial tissues can be readily isolated and possess diverse origins, for example, from surgically removed teeth or gingiva. These cells exhibit stem cell properties, strong potential for self-renewal, and show multi-lineage differentiation, and they have therefore been widely employed in stem cell therapy, tissue regeneration, and inflammatory diseases. Among them, stem cells from human exfoliated deciduous teeth [SHED] and their derivatives have manifested wide application in the treatment of diseases because of their outstanding advantages— including convenient access, easy storage, and less immune rejection. Numerous studies have shown that most diseases are closely associated with inflammation and that inflammatory diseases are extremely destructive, can lead to necrosis of organ parenchymal cells, and can deposit excessive extracellular matrix in the tissues. Inflammatory diseases are thus the principal causes of disability and death from many diseases worldwide. SHED and their derivatives not only exhibit the basic characteristics of stem cells but also exhibit some special properties of their own, particularly with regard to their great potential in inhibiting inflammation and tissue regeneration. SHED therapy may provide a new direction for the treatment of inflammation and corresponding tissue defects. In this review, we critically analyze and summarize the latest findings on the behaviors and functions of SHED, serum‑free conditioned medium from SHED [SHED-CM], and extracellular vesicles, especially exosomes, from SHED [SHED-Exos], and discuss their roles and underlying mechanisms in the control of inflammatory diseases, thus further highlighting additional functions for SHED and their derivatives in future therapies.

Background In March 2021, the supervision group of our hospital inspected the daily work of the outpatient department in the branch and found many problems in the process, such as an excessive number of daily check-up forms, nurses’ confusion regarding the daily check-up process, and the omission of daily check-up items. Therefore, focusing on these problem, our hospital established a quality improvement team to conduct a status survey and perform this study. This study evaluated the feasibility, availability and sustainability of using a daily goals sheet in the routine work of a stomatological outpatient department and investigated the satisfaction of the nursing staff with the sheet. Methods After determining the theme of this study through the status survey, 60 nurses were randomly selected and divided into an experimental group and a control group by a random grouping method. Then, the study was divided into two stages: Applying the PDCA cycle method and following the MECE (Mad Exclusive, Collectively Exhaustive) principle to design, manufacture and apply the daily goals sheet. After the expert group performed Stage one, an analysis of work efficiency and routine omissions and a staff satisfaction survey were carried out. The results of the groups either using the daily goals sheet (n = 30) or not (n = 30) were analysed and compared. Results The average work time of the daily goals sheet group was 15.20 ± 1.70 min, and that of the nondaily goals sheet group was 25.30 ± 2.70 min (P Conclusion The daily goals sheet can make routine work more efficient and convenient in a stomatological outpatient department. It is recommended for use in stomatological outpatient departments or hospitals.

Background Vitamin D receptor (VDR) plays a vital protective role in oral and colonic epithelial cells. Albeit we know that VDR expression is reduced in the mucosal epithelial layers of autoimmune diseases, the mechanism by which VDR is decreased remains elusive. Methods VDR and zinc finger protein 36 (ZFP36) levels in human samples and cell lines were detected by real-time PCR, western blot and immunostaining. Luciferase report assay was used to test cis-elements in VDR gene promoter, real-time PCR was applied to measure mRNA decay and western blot was performed to evaluate protein degradation. RNA affinity chromatography assay was used to test protein-mRNA interaction. Co-immunoprecipitation was used to detect protein–protein interaction. The role of ZFP36 in AU-rich elements (AREs) in the 3′ untranslated region (UTR) of VDR mRNA was also measured by luciferase report assay. Results We identify ZFP36 can bind with the AREs in the 3’UTR of VDR mRNA, leading to mRNA degradation in oral and colonic epithelial cells under inflammatory circumstance. Either ZFP36 protein or AREs of VDR mRNA mutation abolishes this protein-mRNA binding process. After the key amino acid’s mutation, ZFP36 fails to decrease VDR mRNA expression. We also find that VDR physically binds with Y box-binding protein 1 (YBX-1) to block YBX-1’s nuclear translocation and ameliorate cell death in the presence of inflammation. Conclusion These findings provide insights into the cause of VDR decrease in oral and colonic epithelial cells under inflammatory condition and explain how VDR maintains cell viability in these cells.

Cell division is a central process in bacteria and a prerequisite for pathogenicity. Several proteins are involved in this process to ensure the accurate localization and proper function of the division machinery. In Streptococcus mutans, MapZ marks the division sites and position of the Z-ring to regulate cell division; however, whether MapZ deficiency can impair the cariogenic virulence of S. mutans remains unclear. Here, using a phenotypic assay and RNA-seq, we investigated the role of MapZ in cell envelope maintenance, biofilm formation, and stress tolerance in S. mutans. The results show that MapZ is important for normal cell shape and envelope structure, and its deletion causes abnormal septum structure and a thin cell wall. Subsequently, we found that the absence of MapZ leads to a greater level of cell death within 12 h biofilms, but it does not seem to affect biofilm architecture and accumulation. mapZ deletion also results in a decreased acid and osmotic stress tolerance. Furthermore, RNA-seq data reveal that MapZ deficiency causes changes in the expression levels of genes involved in transport systems, sugar metabolism, nature competence, and bacteriocin synthesis. Interestingly, we found that mapZ mutation renders S. mutans more sensitive to chlorhexidine. Taken together, our study suggests that MapZ plays a role in maintaining cell envelope structure and stress tolerance in S. mutans, showing a potential application as a drug target for caries prevention.

OBJECTIVE There are challenges in the treatment of chronic inflammatory diseases of oral mucosa. Both paeoniflorin (PF) and baicalin (BAI) exert anti-inflammatory effects, but the mechanism underlying their combined effects is still unclear. Here, we explored the anti-inflammatory function of the PF-BAI combination in the oral inflammatory response. MATERIALS AND METHODS The CCK-8 assay was used to determine the proliferative capacity of HOKs with PF and BAI. Enzyme-linked immunosorbent (ELISA), Western blotting, reverse transcription polymerase chain reaction, and confocal immunofluorescence were performed to study the anti-inflammatory effects of PF-BAI in LPS-stimulated human oral keratinocytes (HOKs). Immunohistochemistry and ELISA were performed to detect the levels of NF-κB p65, IKKα and IL-6, TNF-α in OLP and healthy tissues. RESULTS Compared to PF or BAI alone, the combination of PF-BAI at 5 µg/ml downregulated secretion of inflammatory cytokines more effectively (p

Background Oral lichen planus (OLP) is known as a chronic inflammatory disease. Our recent studies have suggested that vitamin D/vitamin D receptor (VDR) signaling exerts its protective effects on oral keratinocyte apoptosis by regulating microRNA-802 and p53-upregulated modulator of apoptosis (PUMA), but its roles in oral epithelial inflammatory responses in OLP are still unknown. Herein, we identify lipopolysaccharide (LPS) is able to enhance interferon gamma (IFNγ) and interleukin-1 beta (IL-1β) productions in human oral keratinocytes (HOKs) dependent on hypoxia-inducible factor-1α (HIF-1α). Methods HIF-1α and cytokines levels in HOKs were investigated by real-time PCR and western blotting after LPS challenge. The effects of 1,25(OH)2D3 on LPS-induced HIF-1α and cytokines were tested by real-time PCR, western blotting, siRNA-interference and plasmids transfection techniques. The roles of 1,25(OH)2D3 in regulating HIF-1α levels were investigated using western blotting, siRNA-interference, plasmids transfection and Chromatin Immunoprecipitation (ChIP) assays. Finally, HIF-1α, IFNγ and IL-1β expressions in oral epithelia derived from mice and individuals were measured by real-time PCR, western blotting and immunohistochemical staining. Results As a critical regulator, vitamin D suppresses LPS-induced HIF-1α to block IFNγ and IL-1β productions. Mechanistically, vitamin D inactivates nuclear factor-κB (NF-κB) pathway and up-regulates von Hippel-Lindau (VHL) levels, leading to HIF-1α reduction. Moreover, HIF-1α status of oral epithelia is elevated in VDR−/− mie as well as in VDR-deficient human biopsies, accompanied with increased IFNγ and IL-1β. Conclusion Collectively, this study uncovers an unrecognized roles of vitamin D/VDR signaling in regulating cytokines in oral keratinocytes and reveals the molecular basis of it. Electronic supplementary material The online version of this article (10.1186/s12964-019-0331-9) contains supplementary material, which is available to authorized users.

Objectives Candida albicans and Candida auris strains are common causative species of Candidiasis. The limited number of antifungal drugs and the current situation of resistance to existing antifungals force us to search for new antifungal alternatives. Methods In this work, primary screening of small molecule libraries (Metabolism Compound Library and Epigenetics Compound Library) consisting of 584 compounds against Candida albicans SC5314 was performed. The dose-response assays, XTT assays, scanning electron microscopy and confocal laser scanning microscopy were used to confirm the antifungal activities of the selected compounds against Candida strains. Results Through the primary screening, we identified five compounds (U73122, disulfiram, BSK805, BIX01294, and GSKJ4) that inhibited strains growth ≥ 80% for dose-response assays. Disulfiram was identified as the most potent repositionable antifungal drug with 50% growth inhibition detected at a concentration as low as 1 mg/L. The further results showed the antifungal activity of disulfiram against biofilm formation of Candida strains with a 50% minimum inhibitory concentration ranging from 32 to 128 mg/L. Further observations by scanning electron microscopy and confocal laser scanning microscopy confirmed the destruction of biofilm architecture and the change of biofilm morphology after being exposed to disulfiram. Conclusion The study indicated the potential clinical application of disulfiram as a promising antifungal drug against candidiasis.

Cell-free based therapy is an effective strategy in regenerative medicine as it avoids controversial issues, such as immunomodulation and stability. Recently, exosomes have been explored as a favorable substitution for stem cell therapy as they exhibit multiple advantages, such as the ability to be endocytosed and innate biocompatibility. This study aimed to investigate the effects of stem cells from human exfoliated deciduous teeth (SHED)-derived exosomes (SHED-Exo) on bone marrow stromal cells (BMSCs) osteogenesis and bone recovery. SHED-Exo were isolated, characterized, and applied to the bone loss area caused by periodontitis in a mouse model. We found that the injection of SHED-Exo restored bone loss to the same extent as original stem cells. Without affecting BMSCs proliferation, SHED-Exo mildly inhibited apoptosis. Moreover, SHED-Exo specifically promoted BMSCs osteogenesis and inhibited adipogenesis compared with SHED-derived conditioned medium. The expression of osteogenic marker genes, alkaline phosphatase activity, and Alizarin Red S staining of BMSCs was significantly increased by co-culturing with SHED-Exo. Moreover, Western blot analysis showed that Runx2, a key transcriptional factor in osteogenic differentiation, and p-Smad5 were upregulated upon SHED-Exo stimulation. Expression of the adipogenic marker PPARγ and the amount of lipid droplets decreased when exosomes were present. Low doses of exosomes inhibited the expression of the inflammatory cytokines IL-6 and TNF-α. In conclusion, SHED-Exo directly promoted BMSCs osteogenesis, differentiation, and bone formation. Therefore, exosomes have the potential to be utilized in the treatment of periodontitis and other bone diseases.

MicroRNA-27a/b are small non-coding RNAs which are reported to regulate inflammatory response and cell proliferation. Although some studies have demonstrated that miR-27b is down-regulated in the oral specimens of patients suffering with oral lichen planus (OLP), the molecular mechanism of miR-27b decrease remains a large mystery, and the expression of miR-27a in OLP is not well explored. Here, we demonstrated both miR-27a and miR-27b, compared with healthy controls, were reduced in the oral biopsies, serum and saliva samples derived from OLP patients. The reductions of miR-27a/b were also confirmed in the lipopolysaccharide (LPS)- or activated CD4+ T cell-treated human oral keratinocytes (HOKs). Furthermore, we found vitamin D receptor (VDR) binding sites in the promoters of miR-27a/b genes and verified this finding. We also tested miR-27a/b levels in the oral epithelium from paricalcitol-treated, vitamin D deficient or VDR knockout mice. In the rescue experiments, we confirmed vitamin D and VDR inhibited LPS- or activated CD4+ T cell-induced miR-27a/b reductions in HOKs. In sum, our results show that vitamin D/VDR signaling induces miR-27a/b in oral lichen planus.

Background Oral microbiota is not only important for maintaining oral health but also plays a role in various oral diseases. However, studies regarding microbiome changes in oral lichen planus (OLP) are very limited. To the best of our knowledge, there has been only two studies investigating salivary microbiome changes in OLP. Therefore, the purpose of this study was to identify the characteristic microbial profile in the saliva of OLP patients, with or without erosive lesions, and compare that with recurrent aphthous ulcer (RAU), a common oral immunological disorder that also shows multiple erosive/ulcerative lesions. Whole saliva samples were collected from 20 patients with OLP (erosive E, n = 10 and non-erosive NE, n = 10), 10 patients with RAU (U) and 10 healthy controls (C). DNA was extracted from the saliva samples, and the 16S rDNA gene V4 hypervariable region was analyzed using Illumina sequencing. Results We obtained 4949 operational taxonomic units (OTUs) from the V4 region in all saliva samples. Community composition analysis showed a clear decreased relative abundance of genera Streptococcus and Sphingomonas in saliva from RAU patients when compared to the other three groups. Relative abundance of Lautropia and Gemella were higher in E group, whereas relative abundance of Haemophilus and Neisseria were higher in NE group when compared to C group. Abiotrophia and Oribacterium were higher in OLP (combining E and NE groups), while Eikenella and Aggregatibacter were lower when compared to C group. There was statistically significance in α-diversity between E and RAU groups(p g_Haemophilus might be the potential biomarker in NE group. Conclusions We found that salivary microbiome in erosive OLP was significantly different from that found in RAU; and these changes may be related to the underlying disease process rather than presence of ulcerative/erosive lesions clinically. In addition, our findings in bacterial relative abundance in OLP were significantly different from the previously reported findings, which points to the need for further research in salivary microbiome of OLP.

Summary Interleukin-17 (IL-17) is highly expressed in the epithelial layer of oral lichen planus (OLP), but the underlying mechanism for IL-17 overexpression remains unknown. Here, we identify renin that is induced by NF-κB pathway contributes to the increase of IL-17 in human oral keratinocytes (HOKs). We describe that the release of cellular renin leads to the phosphorylation of Janus kinase 2 (JAK2) protein. The phosphorylated JAK2 recruits and activates the signal transducer and activator of transcription 4 (STAT4) by phosphorylating STAT4's tyrosine residue 693 (Tyr693). The now-activated STAT4 translocates into nucleus and binds to the promoter region of IL-17 gene in HOKs. Genetic interference of renin restores IL-17 levels in OLP cell models. Collectively, our results reveal that renin upregulates IL-17 expression by enhancing STAT4 phosphorylation. This discovery unveils an underpinning by which IL-17 is increased in oral keratinocytes and provides potential targeted therapies for OLP patients., Graphical Abstract, Highlights • NF-κB pathway induces renin expression in oral lichen planus • Renin upregulation promotes IL-17 expression in oral keratinocytes • Renin regulates IL-17 by promoting STAT4 phosphorylation in oral keratinocytes, Oral Medicine; Molecular Biology; Immunology

Vitamin D is known to play a protective role in inflammatory diseases. Although the suppressive effect of vitamin D/vitamin D receptor (VDR) signaling has been shown in the context of oral lichen planus (OLP), the molecular basis of its regulatory function remains poorly understood. Herein, we reported that miR-802 overexpression in OLP could aggravate apoptosis of oral keratinocytes by targeting B-cell lymphoma 2 mRNA. In addition, vitamin D/VDR signaling was able to suppress miR-802 expression in LPS-treated or activated CD4+ T cell-stimulated human oral keratinocytes by blocking NF-κB pathways, thereby inhibiting OLP apoptosis. Consistent with the results in vitro, we showed that miR-802 expression was enhanced in oral keratinocytes from VDR-/- mice, and an inverse correlation between VDR and miR-802 was found in human biopsy specimens of OLP. Collectively, our data suggest that vitamin D/VDR signaling suppresses oral keratinocyte apoptosis by targeting miR-802.-Zhao, B., Xu, N., Li, R., Yu, F., Zhang, F., Yang, F., Ge, X., Li, Y. C., Du, J. Vitamin D/VDR signaling suppresses microRNA-802-induced apoptosis of keratinocytes in oral lichen planus.

To investigate the effect of tooth extraction with antibiotics on atherosclerosis, and to examine the expression of serum interleukin 6(IL-6) and the pathological changes of the carotid artery in chronic periodontitis(CP) rats with or without atherosclerosis(As).A total of 44 SD rats were randomly divided into four groups, group A(normal control), group B(As), group C(CP), group D(CP+As). After model establishment, group C and group D were randomly divided into group C1/D1 (tooth extraction) and group C2/D2(tooth extraction with antibiotics) according to random number table and received the corresponding oral intervention treatment respectively. Serum IL-6 levels were determined by enzyme linked immunosorbent assay(ELISA) respectively one week before the intervention, one week after the first intervention, one, three, five weeks after the second intervention. The pathological changes of the carotid artery were accessed under light microscope.At all sampling time points, the levels of serum IL-6 in group B, C, D were higher than that of group A, with group D1 being increased most obviously, significantly higher than that of group A(P0.001). One week after the second intervention, the content of IL-6 in group C and group D peaked[C1(127.0 ± 29.9) ng/L, C2: (120.6 ± 23.1) ng/L, D1: (175.1 ± 50.8) ng/L, D2: (160.5 ± 37.7) ng/L], and was significantly higher than that of group B[B: (43.4 ± 7.5) ng/L,P0.001]. Then they all had varying degrees of decline, 5 weeks after the second intervention, group C1 and D1 were still higher than that of group B, but group C2 and D2 were lower than that of group B. At all sampling time points, the levels of serum IL- 6 in group C2/D2 were lower than those in group C1/D1, 5 weeks after the second intervention the difference was most obvious and statistically significant(P0.001). Pathology showed that the carotid artery wall in group A was normal. The carotid artery wall was thickened in group B, inflammatory cells and foam cells could be seen, and elastic fibers disordered. The carotid artery wall in group C1 was uneven, foam cells and a small amount of inflammatory cells were visible, and elastic fiber disordered. Obvious thickening was not seen in the carotid artery wall of group C2, a small amount of foam cells and inflammatory cells were found, and elastic fiber mildly disordered. The carotid artery wall in group D1 was obviously uneven, calcium salt deposits were visible in the artery wall, a large amount of inflammatory cells and foam cells could be found, and elastic fiber disordered. Obvious thickening was not seen in the carotid artery wall of group D2, a small amount of inflammatory cells and a large amount of foam cells could be seen, and elastic fiber disordered.Periodontitis and hyperlipidemia could increase the level of serum IL- 6 and the risk of the As. In chronic periodontitis rats with or without atherosclerosis, when periodontal inflammation was not controlled, tooth extraction may increase the risk of the As. At the time of tooth extraction, giving the anti-inflammatory treatment can reduce the risk to a certain extent.

A coral-associated fungus Penicillium sp.gxwz446 that produced exopolysaccharde was isolated from the coral Echinogorgia flora in South China. Two neutral exopolysaccharides GX1-1 and GX2-1 were obtained from the fermented broth of the fungus and purified by anion-exchange and gel-permeation chromatography. Chemical and spectroscopic analyses showed that GX1-1 was a glucan, primarily composed of glucose, with a molecular weight of 5.0 kDa. GX1-1 mainly consists of (1→4)-linked α-d-glucopyranose units as the backbone, substituted at C-2 with a single α-d-glucopyranose on every sixth sugar residues. GX2-1 was a galactofuranose-containing mannogalactoglucan with a molecular weight of 9.5 kDa. The main linkages were composed of (1→4)-β-d-Glcp, (1→5)-β-d-Galf, (1→3,5)-β-d-Galf, (1→6)-α-d-Manp and (1→2, 6)-α-d-Manp. GX1-1 showed RAW264.7 macrophage activation activity. After subjecting GX1-1 to sulfated modification, there was about one sulfate substitution on every sugar ring, primarily at O-6. The sulfated derivative of GX1-1 exhibited a more significant ability to promote the pinocytic activity of RAW264.7 cells and induce the production of NO.

In flying insects, there is frequently a lack of congruence between empirical estimates of local demographic parameters and the prediction that differentiation between populations should decrease with increasing dispersal, a puzzling phenomenon known as Slatkin's Paradox. Here, we generalize Slatkin's Paradox to other taxa, drawing from available information on dispersal to predict the relative importance of pollen vs. seed migration in structuring broad-scale patterns of genetic variation in Ficus hirta, a dioecious fig whose pollen is dispersed by minute, species-specific fig wasps and whose seeds are disseminated by a variety of vagile vertebrates (especially bats and birds). Local-scale observational and genetic studies of dioecious understory figs suggest comparable rates of pollen and seed migration. In contrast, we found unusually low nuclear differentiation (F(ST) =0.037, R(ST) =0.074) and high chloroplast differentiation (G(ST) =0.729, N(ST) =0.798) among populations separated by up to 2850km, leading us to reject the hypothesis of equal pollen and seed migration rates and to obtain an equilibrium estimate of the ratio of pollen to seed migration of r=16.2-36.3. We reconcile this example of Slatkin's Paradox with previously published data for dioecious figs and relate it to the picture of exceptionally long-distance wasp-mediated pollen dispersal that is emerging for large monoecious fig trees. More generally, we argue that Slatkin's Paradox is a general phenomenon and suggest it may be common in plants and animals.