ASFV pA151R negatively regulates type I IFN production via degrading E3 ligase TRAF6.

African swine fever (ASF) caused by African swine fever virus (ASFV) is a highly mortal and hemorrhagic infectious disease in pigs. Previous studies have indicated that ASFV modulates interferon (IFN) production. In this study, we demonstrated that ASFV pA151R negatively regulated type I IFN production. Ectopic expression of pA151R dramatically inhibited K63-linked polyubiquitination and Ser172 phosphorylation of TANK-binding kinase 1 (TBK1). Mechanically, we demonstrated that E3 ligase TNF receptor-associated factor 6 (TRAF6) participated in the ubiquitination of TBK1 in cGAS-STING signaling pathway. We showed that pA151R interacted with TRAF6 and degraded it through apoptosis pathway, leading to the disruption of TBK1 and TRAF6 interaction. Moreover, we clarified that the amino acids H102, C109, C132, and C135 in pA151R were crucial for pA151R to inhibit type I interferon production. In addition, we verified that overexpression of pA151R facilitated DNA virus Herpes simplex virus 1 (HSV-1) replication by inhibiting IFN-ß production. Importantly, knockdown of pA151R inhibited ASFV replication and enhanced IFN-ß production in porcine alveolar macrophages (PAMs). Our findings will help understand how ASFV escapes host antiviral immune responses and develop effective ASFV vaccines.

African swine fever virus S273R protein antagonizes type I interferon production by interfering with TBK1 and IRF3 interaction.

African swine fever (ASF) is originally reported in East Africa as an acute hemorrhagic fever. African swine fever virus (ASFV) is a giant and complex DNA virus with icosahedral structure and encodes a variety of virulence factors to resist host innate immune response. S273R protein (pS273R), as a SUMO-1 specific cysteine protease, can affect viral packaging by cutting polymeric proteins. In this study, we found that pS273R was an important antagonistic viral factor that suppressed cGAS-STING-mediated type I interferon (IFN-I) production. A detailed analysis showed that pS273R inhibited IFN-I production by interacting with interferon regulatory factor 3 (IRF3). Subsequently, we showed that pS273R disrupted the association between TBK1 and IRF3, leading to the repressed IRF3 phosphorylation and dimerization. Deletion and point mutation analysis verified that pS273R impaired IFN-I production independent of its cysteine protease activity. These findings will help us further understand ASFV pathogenesis.

Controllable Crystallization of Two-Dimensional Bi Nanocrystals with Morphology-Boosted CO2 Electroreduction in Wide pH Environments.

Two-dimensional low-melting-point (LMP) metal nanocrystals are attracting increasing attention with broad and irreplaceable applications due to their unique surface and topological structures. However, the chemical synthesis, especially the fine control over the nucleation (reduction) and growth (crystallization), of such LMP metal nanocrystals remains elusive as limited by the challenges of low standard redox potential, low melting point, poor crystalline symmetry, etc. Here, a controllable reduction-melting-crystallization (RMC) protocol to synthesize free-standing and surfactant-free bismuth nanocrystals with tunable dimensions, morphologies, and surface structures is presented. Especially, ultrathin bismuth nanosheets with flat or jagged surfaces/edges can be prepared with high selectivity. The jagged bismuth nanosheets, with abundant surface steps and defects, exhibit boosted electrocatalytic CO2 reduction performances in acidic, neutral, and alkaline aqueous solutions, achieving the maximum selectivity of near unity at the current density of 210 mA cm-2 for formate evolution under ambient conditions. This work creates the RMC pathway for the synthesis of free-standing two-dimensional LMP metal nanomaterials and may find broader applicability in more interdisciplinary applications.

Ultrathin Dendritic Pd-Ag Nanoplates for Efficient and Durable Electrocatalytic Reduction of CO2 to Formate.

CO2 reduction reactions (CO2 RR) powered by renewable electricity can directly convert CO2 to hydrocarbons and fix the sustainable but intermittent energy (e. g., sunlight, wind, etc.) in stable and portable chemical fuels. Advanced catalysts boosting CO2 RR with high activity, selectivity, and durability at low overpotentials are of great importance but still elusive. Here, we report that the ultrathin Pd-Ag dendritic nanoplates (PdAg DNPs) exhibited boosted activity, selectivity, and stability for producing formate from CO2 at a very low overpotential in aqueous solutions under ambient conditions. As a result, the PdAg DNPs exhibited a Faradaic efficiency (FE) for formate of 91% and a cathodic energy efficiency (EE) of ∼90% at the potential of -0.2 V versus reversible hydrogen electrode (vs. RHE), showing significantly enhanced durability as compared with pure Pd catalysts. Our strategy represents a rational catalyst design by engineering the surface geometrical and electronic structures of metal nanocrystals and may find more applicability in future electrocatalysis.

Silver Needle Thermal Therapy Relieves Pain, Repairs the Damaged Myofascial Fiber, and Reduces the Expression of 5-HT3 Receptors in the Spinal Cord of Rats with Myofascial Pain Syndrome.

Background: There is an urgent clinical need to provide a theoretical basis for silver needle thermal therapy to Myofacial pain syndrome (MPS). Objective: This study was conducted to explore the effect of silver needle thermal therapy on myofascial pain syndrome in rats. Methods: MPS rat models were duplicated, and the rats were subsequently divided into model and treatment groups. A normal control group was synchronously set up. No treatment was given to the model group, whereas silver needle thermal therapy was administered to the treatment group. The thermal and mechanical pain threshold, the morphological structure as well as the expression of 5-HT3 receptors in the spinal cord were observed. Results: Rats from the treatment group presented with a significantly higher pain threshold compared to the untreated model group.The myofascial arrangement of the affected part of the model group was disordered, and some muscle fibers were atrophied and deformed. Meanwhile, the myofascial arrangement of the treatment group became more regular than that of the model group. The expression levels of 5-HT3 receptor in the spinal cord of the untreated model group were significantly increased, while being markedly decreased in the treatment group. Conclusions: Silver needle thermal therapy can augment the pain threshold of rats with MPS, repair the damaged myofascial membrane in the rats, and further reduce the expression of 5-HT3 receptors in the spinal cord of the MPS rats.

Host liver-derived extracellular vesicles deliver miR-142a-3p induces neutrophil extracellular traps via targeting WASL to block the development of Schistosoma japonicum.

Schistosomiasis is an important neglected tropical disease. Interactions between the host immune system and schistosomes are complex. Neutrophils contribute to clearance of large pathogens primarily by releasing neutrophil extracellular traps (NETs). However, the functional role of NETs in clearing schistosomes remains unclear. Herein, we report that extracellular vesicles (EVs) derived from the liver of Schistosoma japonicum-infected mice (IL-EVs) induce NET release by delivering miR-142a-3p to target WASL and block the development of S. japonicum. WASL knockout accelerated the formation of NETs that blocked further development of S. japonicum. miR-142a-3p and NETs upregulated the expression of CCL2, which recruits macrophages that block S. japonicum development. However, S. japonicum inhibited NET formation in wild-type mice by upregulating host interleukin-10 (IL-10) expression. In contrast, in WASL knockout mice, IL-10 expression was downregulated, and S. japonicum-mediated inhibition of NET formation was significantly reduced. IL-EV-mediated induction of NET formation is thus an anti-schistosome response that can be counteracted by S. japonicum. These findings suggest that IL-EV-mediated induction of NET formation plays a key role in schistosome infection and that WASL is a potential therapeutic target in schistosomiasis and other infectious diseases.

Controlled Synthesis of Intermetallic Au2 Bi Nanocrystals and Au2 Bi/Bi Hetero-Nanocrystals with Promoted Electrocatalytic CO2 Reduction Properties.

The electrocatalytic properties of metal nanoparticles (NPs) strongly depend on their compositions and structures. Rational design of alloys and/or heterostructures provides additional approaches to modifying their surface geometric and electronic structures for optimized electrocatalytic performance. Here, a solution synthesis of freestanding intermetallic Au2 Bi NPs, the heterostructures of Au2 Bi/Bi hetero-NPs, and their promoted electrocatalytic CO2 reduction reaction (CO2 RR) performances were reported. It was revealed that the formation and in-situ conversion of heterogeneous seeds (e. g., Au) were of vital importance for the formation of intermetallic Au2 Bi and Au2 Bi/Bi hetero-NPs. It was also found that the Au components would act as the structure promoter moderating the binding strength for key intermediates on Bi surfaces. The alloying of Bi with Au and the formation of heterogeneous Au2 Bi/Bi interfaces would create more surface active sites with modulated electronic structures and stronger adsorption strengths for key intermediates, promoting the CO2 -to-HCOOH conversion with high activity and selectivity. This work presents a novel route for preparing intermetallic nanomaterials with modulated surface geometric/electric structures and promoting their electrocatalytic activities with alloying effects and interfacial effects. Such strategy may find wide application in catalyst design and synthesis for more electrocatalytic reactions.

Promoting the Electrocatalytic Reduction of CO2 on Ultrathin Porous Bismuth Nanosheets with Tunable Surface-Active Sites and Local pH Environments.

Electrochemical CO2 reduction reaction (CO2RR) yielding value-added chemicals provides a sustainable approach for renewable energy storage and conversion. Bismuth-based catalysts prove to be promising candidates for converting CO2 and water into formate but still suffer from poor selectivity and activity and/or sluggish kinetics. Here, we report that ultrathin porous Bi nanosheets (Bi-PNS) can be prepared through a controlled solvothermal protocol. Compared with smooth Bi nanoparticles (Bi-NPs), the ultrathin, rough, and porous Bi-PNS provide more active sites with higher intrinsic reactivities for CO2RR. Moreover, such high activity further increases the local pH in the vicinity of the catalyst surfaces during electrolysis and thus suppresses the competing hydrogen evolution reaction. As a result, the Bi-PNS exhibit significantly boosted CO2RR properties, showing a Faradaic efficiency of 95% with an effective current density of 45 mA cm-2 for formate evolution at the potential of -1.0 V versus reversible hydrogen electrode.

Modulating the electrocatalytic CO2 reduction performances of bismuth nanoparticles with carbon substrates with controlled degrees of oxidation.

The catalytic performances of metal nanoparticles can be widely tuned and promoted by the metal-support interactions. Here, we report that the morphologies and electrocatalytic CO2 reduction reaction (CO2RR) properties of bismuth nanoparticles (BiNPs) can be rationally modulated by their interactions with carbon black (CB) supports by controlling the degree of surface oxidation. Appropriately oxidized CB supports can provide sufficient oxygen-containing groups for anchoring BiNPs with tunable sizes and surface areas, desirable key intermediate adsorption abilities, appropriate surface wettability, and adequate electron transfer abilities. As a result, the optimized Bi/CB catalysts exhibited a promoted CO2RR performance with a Faradaic efficiency of 94% and a current density of 16.7 mA cm-2 for HCOO- at -0.9 V versus a reversible hydrogen electrode. Our results demonstrate the significance of regulating the interactions between supports and metal nanoparticles for both synthesis of the catalyst and electrolysis applications, which may find broader applicability in more electrocatalyst designs.

Metal-organic framework membranes with single-atomic centers for photocatalytic CO2 and O2 reduction.

The demand for sustainable energy has motivated the development of artificial photosynthesis. Yet the catalyst and reaction interface designs for directly fixing permanent gases (e.g. CO2, O2, N2) into liquid fuels are still challenged by slow mass transfer and sluggish catalytic kinetics at the gas-liquid-solid boundary. Here, we report that gas-permeable metal-organic framework (MOF) membranes can modify the electronic structures and catalytic properties of metal single-atoms (SAs) to promote the diffusion, activation, and reduction of gas molecules (e.g. CO2, O2) and produce liquid fuels under visible light and mild conditions. With Ir SAs as active centers, the defect-engineered MOF (e.g. activated NH2-UiO-66) particles can reduce CO2 to HCOOH with an apparent quantum efficiency (AQE) of 2.51% at 420 nm on the gas-liquid-solid reaction interface. With promoted gas diffusion at the porous gas-solid interfaces, the gas-permeable SA/MOF membranes can directly convert humid CO2 gas into HCOOH with a near-unity selectivity and a significantly increased AQE of 15.76% at 420 nm. A similar strategy can be applied to the photocatalytic O2-to-H2O2 conversions, suggesting the wide applicability of our catalyst and reaction interface designs.

Sja-miR-71a in Schistosome egg-derived extracellular vesicles suppresses liver fibrosis caused by schistosomiasis via targeting semaphorin 4D.

Schistosomiasis is characterized by liver fibrosis, and studies have indicated that Schistosoma japonicum (S. japonicum) eggs can limit the progression of liver fibrosis. However, the detailed molecular mechanisms are yet unclear. Extracellular vesicles (EVs) contain a selection of miRNAs for long-distance exchange of information and act as an important pathway for host-parasite communication. This study aimed to explore the potential role of S. japonicum egg-derived EVs and its key miRNA in liver fibrosis. Herein, we found that S. japonicum egg-derived EVs can inhibit the activation of hepatic stellate cells, which is mediated via the high expression of Sja-miR-71a. Sja-miR-71a in EVs attenuates the pathological progression and liver fibrosis in S. japonicum infection. Sja-miR-71a inhibiting TGF-ß1/SMAD and interleukin (IL)-13/STAT6 pathways via directly targeting semaphorin 4D (Sema4D). In addition, Sja-miR-71a can also suppress liver fibrosis by regulating Th1/Th2/Th17 and Treg balance. This study contributes to further understanding of the molecular mechanisms underlying Schistosoma-host interactions, and Sema4D may be a potential target for schistosomiasis liver fibrosis treatment.

The genetic basis of adaptive evolution in parasitic environment from the Angiostrongylus cantonensis genome.

Angiostrongylus cantonensis (rat lungworm) is the etiological agent of angiostrongyliasis, mainly causing eosinophilic meningitis or meningoencephalitis in human. Although the biology of A. cantonensis is relatively well known, little is understood about the mechanisms of the parasite's development and survival in definitive hosts, or its adaptation to a broad range of snail intermediate hosts. Here, we generate a high-quality assembly of a well-defined laboratory strain of A. cantonensis from Guangzhou, China, by using Illumina and PacBio sequencing technologies. We undertake comparative analyses with representative helminth genomes and explore transcriptomic data throughout key developmental life-cycles of the parasite. We find that part of retrotransposons and gene families undergo multiple waves of expansions. These include extracellular superoxide dismutase (EC-SOD) and astacin-like proteases which are considered to be associated with invasion and survival of the parasite. Furthermore, these paralogs from different sub-clades based on phylogeny, have different expression patterns in the molluscan and rodent stages, suggesting divergent functions under the different parasitic environment. We also find five candidate convergent signatures in the EC-SOD proteins from flukes and one sub-clade of A. cantonensis. Additionally, genes encoding proteolytic enzymes, involved in host hemoglobin digestion, exhibit expansion in A. cantonensis as well as two other blood-feeding nematodes. Overall, we find several potential adaptive evolutionary signatures in A. cantonensis, and also in some other helminths with similar traits. The genome and transcriptomes provide a useful resource for detailed studies of A. cantonensis-host adaptation and an in-depth understanding of the global-spread of angiostrongyliasis.

Morphology-dependent electrocatalytic nitrogen reduction on Ag triangular nanoplates.

Electrocatalytic nitrogen reduction reactions (ENRR) can produce ammonia from nitrogen and water under ambient conditions. Here, we report the morphology-dependent electro-catalytic nitrogen reduction on Ag triangular nanoplates. Boosted by potassium cations, Ag triangular nanoplates with sharp edges exhibit a high faradaic efficiency of 25% with an ammonia yield of 58.5 mg gAg-1 h-1 at a low overpotential of -0.25 V vs. RHE. In comparison, rounded Ag nanoparticles mainly enclosed by {111} and {100} surfaces show a much smaller faradaic efficiency of 16% and ammonia yield of 38 mg gAg-1 h-1 at a larger overpotential (-0.35 V vs. RHE).

Chi3l3: a potential key orchestrator of eosinophil recruitment in meningitis induced by Angiostrongylus cantonensis.

BACKGROUND: Angiostrongylus cantonensis, an important foodborne parasite, can induce serious eosinophilic meningitis in non-permissive hosts, such as mouse and human. However, the characteristics and mechanisms of the infection are still poorly understood. This study sought to determine the key molecules and its underlying mechanism in inducing brain eosinophilic infiltration caused by Angiostrongylus cantonensis. METHODS: Mathematical models were established for prediction of significantly changing genes and the functional associated protein with RNA-seq data in Angiostrongylus cantonensis infection. The expression level of Chi3l3, the predicted key molecule, was verified using Western blotting and real-time quantitative PCR. Critical cell source of Chi3l3 and its relationship with eosinophils were identified with flow cytometry, immunohistochemistry, and further verified by macrophage depletion using liposomal clodronate. The role of soluble antigens of Angiostrongylus cantonensis in eosinophilic response was identified with mice airway allergy model by intranasal administration of Alternaria alternate. The relationship between Chi3l3 and IL-13 was identified with flow cytometry, Western blotting, and Seahorse Bioscience extracellular flux analyzer. RESULTS: We analyzed the skewed cytokine pattern in brains of Angiostrongylus cantonensis-infected mice and found Chi3l3 to be an important molecule, which increased sharply during the infection. The percentage of inflammatory macrophages, the main source of Chi3l3, also increased, in line with eosinophils percentage in the brain. Network analysis and mathematical modeling predirect a functional association between Chi3l3 and IL-13. Further experiments verified that the soluble antigen of Angiostrongylus cantonensis induce brain eosinophilic meningitis via aggravating a positive feedback loop between IL-13 and Chi3l3. CONCLUSIONS: We present evidences in favor of a key role for macrophave-derived Chi3l3 molecule in the infection of Angiostrongylus cantonensis, which aggravates eosinophilic meningitis induced by Angiostrongylus cantonensis via a IL-13-mediated positive feedback loop. These reported results constitute a starting point for future research of angiostrongyliasis pathogenesis and imply that targeting chitinases and chitinase-like-proteins may be clinically beneficial in Angiostrongylus cantonensis-induced eosinophilic meningitis.

Exosomes Derived from Dendritic Cells Treated with Schistosoma japonicum Soluble Egg Antigen Attenuate DSS-Induced Colitis.

Exosomes are 30-150 nm small membrane vesicles that are released into the extracellular medium via cells that function as a mode of intercellular communication. Dendritic cell (DC)-derived exosomes modulate immune responses and prevent the development of autoimmune diseases. Moreover, Schistosoma japonicum eggs show modulatory effects in a mouse model of colitis. Therefore, we hypothesized that exosomes derived from DCs treated with S. japonicum soluble eggs antigen (SEA; SEA-treated DC exosomes) would be useful for treating inflammatory bowel disease (IBD). Exosomes were purified from the supernatant of DCs treated or untreated with SEA and identified via transmission electron microscopy, western blotting and NanoSight. Acute colitis was induced via the administration of dextran sulfate sodium (DSS) in drinking water (5.0%, wt/vol). Treatment with exosomes was conducted via intraperitoneal injection (i.p.; 50 µg per mouse) from day 0 to day 6. Clinical scores were calculated based on weight loss, stool type, and bleeding. Colon length was measured as an indirect marker of inflammation, and colon macroscopic characteristics were determined. Body weight loss and the disease activity index of DSS-induced colitis mice decreased significantly following treatment with SEA-treated DC exosomes. Moreover, the colon lengths of SEA-treated DC exosomes treated colitis mice improved, and their mean colon macroscopic scores decreased. In addition, histologic examinations and histological scores showed that SEA-treated DC exosomes prevented colon damage in acute DSS-induced colitis mice. These results indicate that SEA-treated DC exosomes attenuate the severity of acute DSS-induced colitis mice more effectively than DC exosomes. The current work suggests that SEA-treated DC exosomes may be useful as a new approach to treat IBD.

rSj16 Protects against DSS-Induced Colitis by Inhibiting the PPAR-α Signaling Pathway.

Background: Epidemiologic studies and animal model experiments have shown that parasites have significant modulatory effects on autoimmune disorders, including inflammatory bowel disease (IBD). Recombinant Sj16 (rSj16), a 16-kDa secreted protein of Schistosoma japonicum (S.japonicum) produced by Escherichia coli (E. coli), has been shown to have immunoregulatory effects in vivo and in vitro. In this study, we aimed to determine the effects of rSj16 on dextran sulfate sodium (DSS)-induced colitis. Methods: DSS-induced colitis mice were treated with rSj16. Body weight loss, disease activity index (DAI), myeloperoxidase (MPO) activity levels, colon lengths, macroscopic scores, histopathology findings, inflammatory cytokine levels and regulatory T cell (Treg) subset levels were examined. Moreover, the differential genes expression after treated with rSj16 were sequenced, analyzed and identified. Results: rSj16 attenuated clinical activity of DSS-induced colitis mice, diminished pro-inflammatory cytokine production, up-regulated immunoregulatory cytokine production and increased Treg percentages in DSS-induced colitis mice. Moreover, DSS-induced colitis mice treated with rSj16 displayed changes in the expression levels of specific genes in the colon and show the crucial role of peroxisome proliferator activated receptor α (PPAR-α) signaling pathway. PPAR-α activation diminished the therapeutic effects of rSj16 in DSS-induced colitis mice, indicating that the PPAR-α signaling pathway plays a crucial role in DSS-induced colitis development. Conclusions: rSj16 has protective effects on DSS-induced colitis, effects mediated mainly by PPAR-α signaling pathway inhibition. The findings of this study suggest that rSj16 may be useful as a therapeutic agent and that PPAR-α may be a new therapeutic target in the treatment of IBD.

Nitric oxide blocks the development of the human parasite Schistosoma japonicum.

Human schistosomiasis, caused by Schistosoma species, is a major public health problem affecting more than 700 million people in 78 countries, with over 40 mammalian host reservoir species complicating the transmission ecosystem. The primary cause of morbidity is considered to be granulomas induced by fertilized eggs of schistosomes in the liver and intestines. Some host species, like rats (Rattus norvegicus), are naturally intolerant to Schistosoma japonicum infection, and do not produce granulomas or pose a threat to transmission, while others, like mice and hamsters, are highly susceptible. The reasons behind these differences are still a mystery. Using inducible nitric oxide synthase knockout (iNOS-/-) Sprague-Dawley rats, we found that inherent high expression levels of iNOS in wild-type (WT) rats play an important role in blocking growth, reproductive organ formation, and egg development in S. japonicum, resulting in production of nonfertilized eggs. Granuloma formation, induced by fertilized eggs in the liver, was considerably exacerbated in the iNOS-/- rats compared with the WT rats. This inhibition by nitric oxide acts by affecting mitochondrial respiration and energy production in the parasite. Our work not only elucidates the innate mechanism that blocks the development and production of fertilized eggs in S. japonicum but also offers insights into a better understanding of host-parasite interactions and drug development strategies against schistosomiasis.

Soluble antigens from the neurotropic pathogen Angiostrongylus cantonensis directly induce thymus atrophy in a mouse model.

The nematode Angiostrongylus cantonensis (A.C.) is a neurotropic pathogen; stage-III larva invade the human (non-permissive host) central nervous system (CNS) to cause eosinophilic meningitis or meningoencephalitis accompanied by immunosuppression. In an A.C.-infectedmouse (another non-permissive host) model, CNS damage-associated T cell immune deficiency and severe inflammation were proposed to result from activation of the hypothalamic-pituitary-adrenal (HPA) axis. However, glucocorticoids are anti-inflammatory agents. Additionally, while defects in thymic stromal/epithelial cells (TECs) are the major reason for thymic atrophy, TECs do not express the glucocorticoid receptor. Therefore, activation of the HPA axis cannot fully explain the thymic atrophy and inflammation. Using an A.C.-infected mouse model, we found that A.C.-infected mice developed severe thymic atrophy with dramatic impairments in thymocytes and TECs, particularly cortical TECs, which harbor CD4+CD8+ double-positive thymocytes. The impairments resulted from soluble antigens (sAgs) from A.C. in the thymuses of infected mice, as intrathymic injection of these sAgs into live mice and the addition of these sAgs to thymic cell culture resulted in thymic atrophy and cellular apoptosis, respectively. Therefore, in addition to an indirect effect on thymocytes through the HPA axis, our study reveals a novel mechanism by which A.C. infection in non-permissive hosts directly induces defects in both thymocytes and TECs via soluble antigens.

[The treatment of otosclerosis using laser assisted stapedotomy with mini incision in external auditory meatus].

OBJECTIVE: To investigate the feasibility of the treatment of otosclerosis using laser stapedotomy with mini incision in the external auditory meatus. METHOD: Thirteen patients(15 ears) with otosclerosis evidence on clinic history. They were all operated using the laser assisted stapedotomy by mini incision in external auditory meatus because of the wide straight canal. Laser resection the tendo musculistapedius and anterior and postrior arch, breaking the articulatioincudostapedia, removing the stapes superstructure, making a hole of 6mm diameter in the rear of stapes footplate by laser drilling, implanting the corresponding length Piston artificial ossicle. RESULT: All the surgeries were successful and the operation time was about one hour. There was only one patient manifested vertigo and nausea after the operation. But the symptoms improved three days later after the expectant treatment. All the incisions were healed in the externals. There was significant difference between the preoperative and postoperative PTA. The air conduct improved in every frequent and the bone conduct improved in 1 kHz, 2 kHz and 4 kHz. CONCLUSION: Laser assisted stapedotomy by mini incision in the external auditory meatus in patients having wide straight canal with otosclerosis can shorten the operation time, minimize the tissue damage, fasten the healing of the incision and reduce the complications postoperatively. In addition, the mini incision is beauty and easy to nurse.

Soluble antigen derived from IV larva of Angiostrongylus cantonensis promotes chitinase-like protein 3 (Chil3) expression induced by interleukin-13.

Angiostrongyliasis caused by Angiostrongylus cantonensis (A. cantonensis) is an emerging food-borne parasitic disease, which refers basically to eosinophilic meningitis. Chitinase-like protein 3 (Chil3), a member of chitinase-like protein family which has chemotactic activity for eosinophils, is reported to be highly upregulated in brain of mouse infected with A. cantonensis. The mechanisms of high expression of Chil3 and the association between A. cantonensis and Chil3 are rarely reported. In order to understand the mechanism of high expression of Chil3 in A. cantonensis-infected mouse, we measured the level of Chil3 in RAW 264.7 and BV2 cell lines stimulated with soluble antigen of A. cantonensis by qPCR and ELISA. To explore the role of Chil3 in inflammation caused by A. cantonensis, we extracted and cultured brain mononuclear cells (BMNCs) and detected the eosinophil chemotactic activity of Chil3 using transwell assay and flow cytometer. Furthermore, we treated the infected mice by injection with rmChil3 and then counted the number of larvae in brains of infected mice and treated mice to examine the association between the worm and Chil3. Our results showed the soluble antigen from A. cantonensis could promote the Chil3 expression in macrophage and microglial cell lines induced by interleukin-13. In conclusion, we supposed that high expression of Chil3 enhanced by soluble antigens from A. cantonensis might be the reason of serious eosinophil infiltration in mouse brain after A. cantonensis infection.