The protective role of HMGB1 in affecting the balance between autophagy and pyroptosis to maintain neutrophils homeostasis during ß-glucan-induced mice lung inflammation.

Fungal contamination is omnipresent, and inhalation of fungi-contaminated organic dust leads to hypersensitivity pneumonitis (HP), in which neutrophils played a pivotal role. Existing studies have suggested that cell homeostasis is crucial for the pathogenesis of the inflammatory disease. Although HMGB1 has been shown to contribute to suppressing HP, there is a lack of studies on its mechanisms, especially the regulation of neutrophil homeostasis. This study aims to investigate how HMGB1 regulates neutrophil function by affecting neutrophil homeostasis, and then affects lung inflammation induced by ß-glucan, the exposure marker of fungi. Our results showed that deficient HMGB1 led to neutrophil death by disrupting the balance between autophagy and pyroptosis after ß-glucan treatment. And HMGB1 deficiency exacerbated the ß-glucan-induced lung inflammation and neutrophil dysfunction both in vivo and in vitro. Furthermore, HMGB1 contributed to remodeling neutrophil function by restricting autophagy and aggravating pyroptosis ß-glucan exposure. Our funding suggested that HMGB1 deficiency could break the balance between autophagy and pyroptosis towards pyroptosis to cause neutrophil dysfunction during the exacerbated inflammatory response, which provides insights into the pathogenesis of HP and the potential biological targets for its treatment. DATA AVAILABILITY: The datasets used during the current study are available from the corresponding author on reasonable request.

Occupational noise exposure and the prevalence of dyslipidemia in a cross-sectional study.

BACKGROUND: Occupational noise exposure was related to cardiovascular disease, of which dyslipidemia was an important inducement. This study investigated the relationship between occupational noise exposure and dyslipidemia. METHODS: Four hundred ninety-two occupational noise-exposed workers and 664 non-exposed workers were recruited to conduct environmental noise tests and personal occupational physical examinations. A lasso-logistic regression model was used to estimate the relative risk of dyslipidemia. A restricted cubic spline was used to estimate the association between noise exposure years and dyslipidemia after adjusting for potential confounding factors. RESULTS: A crude association was observed between the occupational noise exposure (75-85 dB(A)) and dyslipidemia. After adjusting for confounding factors, there was a non-linear relationship between noise exposure years and dyslipidemia (P for non-linearity =0.01). Workers exposed to 75-85 dB(A) for 11 to 24.5 years had a higher risk of dyslipidemia than non-exposed workers. CONCLUSIONS: A positive and non-linear exposure-response relationship was found in workers exposed to 75-85 dB(A) whose exposure years were between 11 and 24.5. Workers had the highest risk of dyslipidemia when exposed for 13.5 years.

HMGB1 could restrict 1,3-ß-glucan induced mice lung inflammation by affecting Beclin1 and Bcl2 interaction and promoting the autophagy of epithelial cells.

Fungi were microorganisms that are ubiquitous in a variety of environments. Inhalation of fungi-contaminated organic dust led to hypersensitivity pneumonitis and might eventually cause irreversible pulmonary fibrosis. Studies showed that maintaining the homeostasis of epithelial cells was vital for defending the exogenous fungi invasion. HMGB1-dependent autophagy played a critical role in maintaining cell homeostasis in multiple inflammatory diseases. However, the actual role of HMGB1-dependent autophagy in hypersensitivity pneumonitis was unclear. In our study, mice were exposed to 0.3 mg/50 µL 1,3-ß-glucan solution by intratracheal instillation to set up the lung inflammation model. To investigate the role of HMGB1-dependent autophagy in 1,3-ß-glucan induced lung inflammation, AAV-sh-HMGB1 was intratracheally injected to silence HMGB1 in the lung. Our finding suggested that silencing HMGB1 could aggravate the 1,3-ß-glucan induced lung inflammation by inhibiting the autophagy of epithelial cells. And ubiquitination of Beclin1 contributed to decreasing the interaction of Beclin1 and Bcl2, which might be a key regulatory mechanism of HMGB1 on 1,3-ß-glucan induced autophagy.

Arsenic represses airway epithelial mucin expression by affecting retinoic acid signaling pathway.

Arsenic is a ubiquitous environmental toxicant, found in high concentrations worldwide. Although abundant research has dealt with arsenic-induced cancers, studies on mechanisms of non-malignant lung diseases have not been complete. In addition, decades of research have mostly concentrated on high-dose arsenic exposure, which has very limited use in modeling the biological effects of today's low-dose exposures. Indeed, accumulated evidence has shown that low-dose arsenic exposure (i.e. ≤100 ppb) may also alter lung homeostasis by causing host susceptibility to viral infection. However, the underlying mechanism of this alteration is unknown. In this study, we found that low-dose sodium arsenite (As (III)) repressed major airway mucins-MUC5AC and MUC5B at both mRNA and protein levels. We further demonstrated that this repression was not caused by cellular toxicity or mediated by the reduction of a common mucin-inducing pathway-EGFR. Other established mucin activators- dsRNA, IL1ß or IL17 were not able to override As (III)-induced mucin repression. Interestingly, the suppressing effect of As (III) appeared to be partially reversible, and supplementation of all trans retinoic acid (t-RA) doses dependently restored mucin gene expression. Further analyses indicated that As (III) treatment significantly reduced the protein level of retinoic acid receptors (RARα, γ and RXRα) as well as RARE promoter reporter activity. Therefore, our study fills in an important knowledge gap in the field of low-dose arsenic exposure. The interference of RA signaling, and mucin gene expression may be important pathogenic factors in low-dose arsenic induced lung toxicity.

Correction to: Prokaryotic expression and action mechanism of antimicrobial LsGRP1C recombinant protein containing a fusion partner of small ubiquitin-like modifier.

The published online version contains editing mistake in Table 2. See below for the corrected Table.

[Correlation of serum androgen levels with lipid metabolism in middle-aged and elderly men in Zunyi, Guizhou].

OBJECTIVE: To investigate the relationship of the levels of serum androgens with lipid metabolism in middle-aged and elderly men in Zunyi, Guizhou. METHODS: Using the stratified cluster sampling method, we conducted a questionnaire investigation and physical examinations among 437 men in Zunyi City. We divided the subjects into a middle-aged (40－64 ï¼»53.20 ± 7.41ï¼½ years, n = 269) and an elderly group (=≥65 ï¼»70.63 ± 4.66ï¼½ years, n = 168) and collected fasting elbow venous blood samples from them for measuring the levels of total testosterone (TT), sex hormone-binding globulin (SHBG), luteinizing hormone (LH), total cholesterol (TCH), triglyceride (TG), high-density lipoprotein (HDL), low-density lipoprotein (LDL), calculated free testosterone (cFT), free testosterone index (FTI), and testosterone secretion index (TSI). RESULTS: Compared with the elderly group, the middle-aged males showed significantly lower SHBG, LH, HDL and LDL, and higher cFT, FTI, TSI, TG and TCH (all P < 0.05). TT and SHBG were negatively correlated with TG, TCH, HDL and LDL, while cFT was positively correlated with TCH, and so was FTI with TG, TCH with LDL, and TSI with TCH, HDL and LDL (all P < 0.05), but LH was negatively correlated with TG, TCH and LDL (all P < 0.05). Multivariate linear regression analysis showed that TT and SHBG were negatively correlated with TG, TCH, HDL and LDL, and so was LH with TCH, HDL and LDL (all P < 0.05). CONCLUSIONS: In the middle-aged and elderly men in Zunyi, low concentrations of TT, SHBG and LH were associated with the increased risk of high-TCH and -LDL dyslipidemia, low concentrations of TT and SHBG with that of high-TG dyslipidemia, while high concentrations of TT, SHBG and LH with that of low-HDL dyslipidemia.

Prokaryotic expression and action mechanism of antimicrobial LsGRP1C recombinant protein containing a fusion partner of small ubiquitin-like modifier.

Antimicrobial peptides (AMPs) are peptides exhibiting broad-spectrum antimicrobial activities and considered as potential therapeutic agents. LsGRP1C, a novel AMP derived from defense-related LsGRP1 protein of Lilium, was proven to inhibit kinds of bacteria and fungi via alteration of microbial membrane permeability and induction of fungal programmed cell death-like phenomena by in vitro assays using synthetic LsGRP1C. In this study, the prokaryotic production of LsGRP1C recombinant protein containing an N-terminal fusion partner of the yeast small ubiquitin-like modifier (SUMO) was achieved by using optimized Escherichia coli host and purification buffer system, which lead to a high yield of soluble SUMO-LsGRP1C fusion protein. In vitro assay revealed that E. coli-expressed SUMO-LsGRP1C exhibited even better antifungal activity as compared to synthetic LsGRP1C. Meanwhile, the ability of SUMO-LsGRP1C in conducting fungal membrane permeabilization and programmed cell death was verified by SYTOX Green staining and 4',6-diamidino-2-phenylindole staining/terminal deoxynucleotidyl transferase dUTP nick-end labeling assays, respectively, indicating that E. coli-expressed SUMO-LsGRP1C shares identical modes of action with synthetic LsGRP1C. Herein, this E. coli expression system enables the effective and convenient production of antimicrobial LsGRP1C in a form of SUMO-fused recombinant protein.

IL-10-Producing B Cells Suppress Effector T Cells Activation and Promote Regulatory T Cells in Crystalline Silica-Induced Inflammatory Response In Vitro.

Long-term exposure to crystalline silica leads to silicosis, which is characterized by persistent lung inflammation and lung fibrosis. Multiple immune cells have been demonstrated to participate in crystalline silica-induced immune responses. Our previous study indicated that B10 could control lung inflammation through modulating the Th balance in experimental silicosis in mice. However, the regulatory mechanism of B10 on CD4+ T cells is still unclear. MACS-sorted CD19+ B cells from the three different groups were cultured with CD4+ T cells either with or without transwell insert plates to evaluate the effects of B10 on CD4+ T cells, including Teff and Treg. B10 was eliminated by anti-CD22 application in vivo. Flow cytometry was used to test the frequencies of CD4+ T cells, and the expressions of the related cytokines were detected by real-time PCR and CBA. Insufficient B10 elevated the levels of proinflammatory cytokines and promoted Th responses in a way independent upon cell-cell contact in the Teff and B cell coculture system. B10 could both increase Treg activity and enhance conversion of Teff into Treg. Our findings demonstrated that B10 could affect Th responses by the release of IL-10, enhancing Treg functions and converting Teff into Treg.

[Vasectomy has no obvious longterm influence on the levels of serum androgens in aging males].

OBJECTIVE: To explore the longterm influence of vasectomy on the levels of serum androgens in aging males. METHODS: Using stratified random sampling, we conducted a questionnaire survey and physical examinations among 437 adult males aged ≥40 years, 232 with and 205 without the history of vasectomy. In addition, we measured the levels of serum total testosterone (TT), sexhormone binding globulin (SHBG), calculated free testosterone (cFT), testosterone secreting index (TSI), free testosterone index (FTI), and luteinizing hormone (LH). RESULTS: Compared with the nonvasectomy group, the vasectomy group showed significantly increased levels of serum TT (ï¼»16.01±5.41ï¼½ vs ï¼»17.39±6.57ï¼½ nmol/L), SHBG (ï¼»58.91±36.89ï¼½ vs ï¼»70.28±40.90ï¼½ nmol/L), and LH (ï¼»8.86±6.49ï¼½ vs ï¼»10.85±11.73ï¼½ IU/L) (all P< 0.05) and a decreased level of FTI (0.33±0.15 vs 0.30±0.12, P< 0.05). There were no statistically significant differences between the nonvasectomy and vasectomy groups in cFT (ï¼»0.24±0.07ï¼½ vs ï¼»0.23±0.09ï¼½ nmol/L) or TSI (ï¼»2.42±1.34ï¼½ vs ï¼»2.46±1.51ï¼½ nmol/IU) (both P>0.05), nor after adjustment for relevant factors in TT (ß: 1.015, 95% CI: －0.180－2.210), SHBG (ß: 5.118, 95% CI: －2.069－12.305), cFT (ß: 0.003, 95% CI: －0.011－0.018), FTI (ß: －0.012, 95% CI: －0.035－0.011), TSI (ß: 0.138, 95% CI: －0.131－0.407), and LH (ß: 1.011, 95% CI: －0.811－2.834) (all P>0.05). CONCLUSIONS: Vasectomy has no obvious longterm influence on the levels of serum androgens in aging males.

A Phosphorescent Platinum(II) Bipyridyl Supramolecular Polymer Based on Quadruple Hydrogen Bonds.

A platinum(II) bipyridyl complex bearing bis-ureidopyrimidinone (Pt-bisUPy) has been designed and its self-assembling behavior has been thoroughly investigated by 1 H NMR, DOSY NMR, Ubbelohde viscometry analysis, UV/Vis, and emission spectroscopies. Pt-bisUPy underwent concentration-dependent ring-chain polymerization in apolar solvents. Hydrogen-bonding interactions play an important role during the formation of the supramolecular polymers. Hydrogen-bonded supramolecular polymers were transformed to nanoparticles in water through the miniemulsion method. These nanoparticles showed strong π-π excimeric emission. Metal-metal-to-ligand charge transfer (MMLCT) from Pt-Pt interactions was not significant in the emission spectrum. The phosphorescence of the nanoparticle persisted even under aerobic conditions. The triplet state of these phosphorescent nanomaterials were long-lived and possessed moderate emission quantum yields. Furthermore, the low toxicity of these materials promises a place for them in in vitro and in vivo bioimaging.

Seasonality of Ankle Swelling: Population Symptom Reporting Using Google Trends.

In our experience, complaints of ankle swelling are more common in summer, typically from patients with no obvious cardiovascular disease. Surprisingly, this observation has never been reported. To objectively establish this phenomenon, we sought evidence of seasonality in the public's Internet searches for ankle swelling. Our data, obtained from Google Trends, consisted of all related Google searches in the United States from January 4, 2004, to January 26, 2016. Consistent with our expectations and confirmed by similar data for Australia, Internet searches for information on ankle swelling are highly seasonal (highest in midsummer), with seasonality explaining 86% of search volume variability.

Blockade of Wnt/ß-Catenin Pathway Aggravated Silica-Induced Lung Inflammation through Tregs Regulation on Th Immune Responses.

CD4(+) T cells play an important role in regulating silica-induced inflammation and fibrosis. Recent studies showed that Wnt/ß-catenin pathway could modulate the function and the differentiation of CD4(+) T cells. Therefore, Wnt/ß-catenin pathway may participate in the development and progress of silicosis. To investigate the role of Wnt/ß-catenin pathway, we used lentivirus expressing ß-catenin shRNA to block the Wnt/ß-catenin pathway by intratracheal instillation to the mice model of silicosis. Treatment of lentivirus could significantly aggravate the silica-induced lung inflammation and attenuated the fibrosis at the late stage. By analyzing CD4(+) T cells, we found that blockade of Wnt/ß-catenin pathway suppressed regulatory T cells (Tregs). Reciprocally, enhanced Th17 response was responsible for the further accumulation of neutrophils and production of proinflammatory cytokines. In addition, blockade of Wnt/ß-catenin pathway delayed the Th1/Th2 polarization by inhibiting Tregs and Th2 response. These results indicated that Wnt/ß-catenin pathway could regulate Tregs to modulate Th immune response, which finally altered the pathological character of silicosis. Our study suggested that Wnt/ß-catenin pathway might be a potential target to treat the silica-induced inflammation and fibrosis.

Baicalin Alleviates Silica-Induced Lung Inflammation and Fibrosis by Inhibiting the Th17 Response in C57BL/6 Mice.

Silicosis is an inflammatory and fibrotic lung disease caused by inhalation of silica. Th17 cells play a key role in causing silica-induced lung inflammation and fibrosis. Baicalin, a compound isolated from the Chinese herb Huangqin, could suppress the differentiation of Th17 cells and alleviate inflammation. However, there are very few reports of the immunoregulatory mechanisms of baicalin in experimental silica-induced lung inflammation and fibrosis. In our study, mice were exposed to silica by intratracheal instillation, and in this way we established an experimental silicosis model. To elucidate the effects and mechanisms of baicalin in silica-induced inflammation and fibrosis, we used baicalin to treat the developed mouse model of silicosis. Treatment with baicalin attenuated the accumulation of inflammatory cells and led to milder pathological inflammatory and fibrotic changes in lung tissues. Baicalin affected the immunological balance between Th17 and Treg responses. Therefore, baicalin caused a decrease in Th17 cells by stimulating Treg cells and by inhibiting IL-6 and IL-23. We further demonstrated that silica-induced Th1 and Th2 immune responses were both inhibited by increased Treg activation, which was promoted by baicalin. Our findings confirmed the potential functions of baicalin in inhibiting the Th17 response and reducing silica-induced inflammation and fibrosis.

Th17 can regulate silica-induced lung inflammation through an IL-1ß-dependent mechanism.

Silicosis is an occupational lung disease caused by the inhalation of silica dust and characterized by lung inflammation and fibrosis. Interleukin (IL)-1ß is induced by silica and functions as the key pro-inflammatory cytokine in this process. The Th17 response, which is induced by IL-1ß, has been reported very important in chronic human lung inflammatory diseases. To elucidate the underlying mechanisms of IL-1ß and IL-17 in silicosis, we used anakinra and an anti-IL-17 monoclonal antibody (mAb) to block the receptor of IL-1ß (IL-RI) and IL-17, respectively, in a mouse model of silicosis. We observed increased IL-1ß expression and an enhanced Th17 response after silica instillation. Treatment with an IL-1 type I receptor (IL-1RI) antagonist anakinra substantially decreased silica-induced lung inflammation and the Th17 response. Lung inflammation and the accumulation of inflammatory cells were attenuated in the IL-17-neutralized silicosis group. IL-17 may promote lung inflammation by modulating the differentiation of Th1 and regulatory T cells (Tregs) and by regulating the production of IL-22 and IL-1ß during the lung inflammation of silicosis. Silica may induce IL-1ß production from alveolar macrophages and promote inflammation by initiating a Th17 response via an IL-1ß/IL-1RI-dependent mechanism. The Th17 response could induce lung inflammation during the pathogenesis of silicosis by regulating the homoeostasis of the Th immune responses and affecting the production of IL-22 and IL-1ß. This study describes a potentially important inflammatory mechanism of silicosis that may bring about novel therapies for this inflammatory and fibrotic disease.

Neutralization of interleukin-17A delays progression of silica-induced lung inflammation and fibrosis in C57BL/6 mice.

Silica exposure can cause lung inflammation and fibrosis, known as silicosis. Interleukin-17A (IL-17A) and Th17 cells play a pivotal role in controlling inflammatory diseases. However, the roles of IL-17A and Th17 cells in the progress of silica-induced inflammation and fibrosis are poorly understood. This study explored the effects of IL-17A on silica-induced inflammation and fibrosis. We used an anti-mouse IL-17A antibody to establish an IL-17A-neutralized mice model, and mice were exposed to silica to establish an experimental silicosis model. We showed that IL-17A neutralization delayed neutrophil accumulation and progression of silica-induced lung inflammation and fibrosis. IL-17A neutralization reduced the percentage of Th17 in CD4+ T cells, decreased IL-6 and IL-1ß expression, and increased Tregs at an early phase of silica-induced inflammation. Neutralization of IL-17A delayed silica-induced Th1/Th2 immune and autoimmune responses. These results suggest that IL-17A neutralization alleviates early stage silica-induced lung inflammation and delays progression of silica-induced lung inflammation and fibrosis. Neutralization of IL-17A suppressed Th17 cell development by decreasing IL-6 and/or IL-1ß and increased Tregs at an early phase of silica-induced inflammation. Neutralization of IL-17A also delayed the Th1/Th2 immune response during silica-induced lung inflammation and fibrosis. IL-17A may play a pivotal role in the early phase of silica-induced inflammation and may mediate the Th immune response to influence silica-induced lung inflammation and fibrosis in mice.

Evolution of oxidation dynamics of histidine: non-reactivity in the gas phase, peroxides in hydrated clusters, and pH dependence in solution.

Oxidation of histidine by (1)O2 is an important process associated with oxidative damage to proteins during aging, diseases and photodynamic therapy of tumors and jaundice, and photochemical transformations of biological species in the troposphere. However, the oxidation mechanisms and products of histidine differ dramatically in these related environments which range from the gas phase through aerosols to aqueous solution. Herein we report a parallel gas- and solution-phase study on the (1)O2 oxidation of histidine, aimed at evaluating the evolution of histidine oxidation pathways in different media and at different ionization states. We first investigated the oxidation of protonated and deprotonated histidine ions and the same systems hydrated with explicit water molecules in the gas phase, using guided-ion-beam-scattering mass spectrometry. Reaction coordinates and potential energy surfaces for these systems were established on the basis of density functional theory calculations, Rice-Ramsperger-Kassel-Marcus modeling and direct dynamics simulations. Subsequently we tracked the oxidation process of histidine in aqueous solution under different pH conditions, using on-line UV-Vis spectroscopy and electrospray mass spectrometry monitoring systems. The results show that two different routes contribute to the oxidation of histidine depending on its ionization states. In each mechanism hydration is essential to suppressing the otherwise predominant dissociation of reaction intermediates back to reactants. The oxidation of deprotonated histidine in the gas phase involves the formation of 2,4-endoperoxide and 2-hydroperoxide of imidazole. These intermediates evolve to hydrated imidazolone in solution, and the latter either undergoes ring-closure to 6α-hydoxy-2-oxo-octahydro-pyrrolo[2,3-d]imidazole-5-carboxylate or cross-links with another histidine to form a dimeric product. In contrast, the oxidation of protonated histidine is mediated by 2,5-endoperoxide and 5-hydroperoxide, which convert to stable hydrated imidazolone end-product in solution. The contrasting mechanisms and reaction efficiencies of protonated vs. deprotonated histidine, which lead to pH dependence in the photooxidation of histidine, are interpreted in terms of the chemistry of imidazole with (1)O2. The biological implications of the results are also discussed.

Reduction of IL-17A might suppress the Th1 response and promote the Th2 response by boosting the function of Treg cells during silica-induced inflammatory response in vitro.

Silica inhalation can induce chronic lung inflammation and fibrosis. Upon silica stimulation, activated macrophages trigger the T-lymphocyte which can differentiate into many different types of Th cells, including the recently discovered Th17 cells. IL-17A, the typical Th17 cytokine, is reported in some inflammatory diseases. However, the role of IL-17A in silica-induced inflammatory response is still not clear. The regulatory mechanism of silica-induced Th17 response also needs to be investigated. So we established a mice primary cell coculture system (macrophage and lymphocyte) to investigate the role of IL-17A in silica-induced inflammatory response in vitro, by using anti-IL-17A mAb and IL-1Ra. Both anti-IL-17A mAb and IL-1Ra decreased the level of IL-17A and increased the function of Treg cells. The Th1 response was suppressed and the Th2 response was promoted by the addition of anti-IL-17A mAb or IL-1Ra. IL-1Ra treatment decreased the level of IL-6, whereas the levels of IL-23 and ROR- γ t were increased. Our study demonstrated that IL-17A reduction altered the pattern of silica-induced Th responses by boosting the function of Treg cells in vitro. Blocking the function of IL-1 signal pathway could suppress the level of IL-17A, which played the major role in modulating silica-induced Th responses in vitro.

lncRNA Profiling of Exosomes and Its Communication Role in Regulating Silica-Stimulated Macrophage Apoptosis and Fibroblast Activation.

Long-term silica particle exposure leads to interstitial pulmonary inflammation and fibrosis, called silicosis. Silica-activated macrophages secrete a wide range of cytokines resulting in persistent inflammation. In addition, silica-stimulated activation of fibroblast is another checkpoint in the progression of silicosis. The pathogenesis after silica exposure is complex, involving intercellular communication and intracellular signaling pathway transduction, which was ignored previously. Exosomes are noteworthy because of their crucial role in intercellular communication by delivering bioactive substances, such as lncRNA. However, the expression profile of exosomal lncRNA in silicosis has not been reported yet. In this study, exosomes were isolated from the peripheral serum of silicosis patients or healthy donors. The exosomal lncRNAs were profiled using high-throughput sequencing technology. Target genes were predicted, and functional annotation was performed using differentially expressed lncRNAs. Eight aberrant expressed exosomal lncRNAs were considered to play a key role in the process of silicosis according to the OPLS-DA. Furthermore, the increased expression of lncRNA MSTRG.43085.16 was testified in vitro. Its target gene PARP1 was critical in regulating apoptosis based on bioinformatics analysis. In addition, the effects of exosomes on macrophage apoptosis and fibroblast activation were checked based on a co-cultured system. Our findings suggested that upregulation of lncRNA MSTRG.43085.16 could regulate silica-induced macrophage apoptosis through elevating PARP1 expression, and promote fibroblast activation, implying that the exosomal lncRNA MSTRG.43085.16 might have potential as a biomarker for the early diagnosis of silicosis.

3-D real-time ultrasound tracking of acoustically actuated swimming microdrone.

Maneuverable microswimmers/microdrones that navigate in hard-to-reach spaces inside human bodies hold a great potential for various biomedical applications. Acoustically actuated microswimmers have already demonstrated feasibility. However, for eventual translation of this technology, a robust 3-D tracking strategy for the microswimmer is particularly required. This paper presents our lab-designed 3-D ultrasound tracking system for real-time tracking of an acoustically actuated 3-D swimming microdrone. The ultrasound tracking system utilizing two ultrasound probes, a step motor and a host controller, was built to track the 3-D arbitrary motion of the microdrone in real-time. The performance of tracking was evaluated in the benchtop experiments by comparing the reconstructed trajectories with synchronized camera recordings. The ultrasound tracking system showed high reliability, with an average error of less than 0.3 mm across six different trials when compared to camera tracking. The results demonstrated the capability of our lab-designed 3-D ultrasound tracking system in accurately tracking the undetermined motion of the acoustic actuated 3-D swimming microdrone in real-time. The developed tracking system holds promise as a potential approach for biomedical applications and could pave the way for future clinical translation of the microswimmer technology.