In vivo endoscopic ultrasound imaging with a rotational-scanning, all-optical ultrasound probe.

All-optical ultrasound manipulates ultrasound waves based on laser and photonics technologies, providing an alternative approach for pulse-echo ultrasound imaging. However, its endoscopic imaging capability is limited ex vivo by the multifiber connection between the endoscopic probe and the console. Here, we report on all-optical ultrasound for in vivo endoscopic imaging using a rotational-scanning probe that relies on a small laser sensor to detect echo ultrasound waves. The acoustically induced lasing frequency change is measured via heterodyne detection by beating the two orthogonally polarized laser modes, enabling a stable output of ultrasonic responses and immunity to low-frequency thermal and mechanical disturbances. We miniaturize its optical driving and signal interrogation unit and synchronously rotate it with the imaging probe. This specialized design leaves a single-fiber connection to the proximal end and allows fast rotational scanning of the probe. As a result, we used a flexible, miniature all-optical ultrasound probe for in vivo rectal imaging with a B-scan rate of 1 Hz and a pullback range of ∼7 cm. This can visualize the gastrointestinal and extraluminal structures of a small animal. This imaging modality offers an imaging depth of 2 cm at a central frequency of ∼20 MHz, showing promise for high-frequency ultrasound imaging applications in gastroenterology and cardiology.

Three new long-chain polyenes from the mangrove-derived fungus Penicillium herquei JX4.

One new epimer pair of long-chain polyenes penicilqueis E (1) and F (2), and one new long-chain polyene pinophol G (3), along with one known compound (4), were obtained from EtOAc extract of the mangrove-derived fungus Penicillium herquei JX4. Their structures were elucidated by detailed analysis of comprehensive spectroscopic data. The inhibitory activities of all compounds against the nitric oxide (NO) production induced by lipopolysaccharide in mouse macrophage RAW 264.7 cells in vitro were evaluated.

Cochlin produced by follicular dendritic cells promotes antibacterial innate immunity.

Cochlin, an extracellular matrix protein, shares homologies with the Factor C, a serine protease found in horseshoe crabs, which is critical for antibacterial responses. Mutations in the COCH gene are responsible for human DFNA9 syndrome, a disorder characterized by neurodegeneration of the inner ear that leads to hearing loss and vestibular impairments. The physiological function of cochlin, however, is unknown. Here, we report that cochlin is specifically expressed by follicular dendritic cells and selectively localized in the fine extracellular network of conduits in the spleen and lymph nodes. During inflammation, cochlin was cleaved by aggrecanases and secreted into blood circulation. In models of lung infection with Pseudomonas aeruginosa and Staphylococcus aureus, Coch(-/-) mice show reduced survival linked to defects in local cytokine production, recruitment of immune effector cells, and bacterial clearance. By producing cochlin, FDCs thus contribute to the innate immune response in defense against bacteria.

[Establishment of a system for regulating the gene expression of embryonic mouse cerebral cortex neural stem cells by in utero electroporation]. / å­å®«å† ç”µç©¿å­”æ³•è°ƒæŽ§é¼ èƒšå¤§è„‘çš®è´¨ç¥žç»å¹²ç»†èƒžåŸºå› è¡¨è¾¾ä½“ç³»çš„å»ºç«‹.

OBJECTIVES: To establish a system for regulating the gene expression of embryonic mouse cerebral cortex neural stem cells (NSCs) using in utero electroporation (IUE). METHODS: At embryonic day 14.5, the mouse cerebral cortex NSCs were electro-transfected with the pCIG plasmid injected into the ventricle of the mouse embryo. At embryonic day 16.5 or day 17.5, embryonic mouse brain tissues were collected to prepare frozen sections. Immunofluorescence staining was used to observe the proliferation, apoptosis, division, directional differentiation, migration, and maturation of NSCs. RESULTS: The differentiation of NSCs into intermediate progenitors, the proliferation and apoptosis of NSCs, and the morphological development of radial axis of radial glial cells were observed at embryonic day 16.5. The differentiation of NSCs into neurons in layers V-VI of the cerebral cortex, the migration of NSCs to the lateral cerebral cortex, the development of dendrites of migrating neurons, and the maturation of neurons were observed at embryonic day 17.5. CONCLUSIONS: The system for regulating the gene expression of embryonic mouse cerebral cortex NSCs can be established using IUE, which is useful for the study of neural development related to the proliferation, apoptosis, division, directional differentiation, migration and maturation of NSCs in the cerebral cortex.

Long non-coding RNA MCF2L-AS1 promotes the aggressiveness of colorectal cancer by sponging miR-874-3p and thereby up-regulating CCNE1.

BACKGROUND: Long non-coding RNAs (lncRNAs) have drawn growing attention because of the role which they play in various diseases, including colorectal cancer (CRC). However, the potential functions of lncRNA MCF2L antisense RNA 1 (MCF2L-AS1) in tumors remained largely unclear. The present study aimed to explore the clinical significance and the biological effects of lncRNA MCF2L antisense RNA 1 (MCF2L-AS1) in CRC. METHODS: Reverse transcriptase-polymerase chain reaction was performed to determine the expression of MCF2L-AS1 in CRC. The clinical significance of MCF2L-AS1 in CRC patients was analyzed statistically. In vitro experiments were performed to determine the effects of MCF2L-AS1 on the cellular progression of CRC cells. Bioinformatic assays, luciferase reporter assays and RNA-pulldown assays were performed to predict for potential microRNAs that can interact with MCF2L-AS1 and mRNAs that can interact with miR-874-3p. RESULTS: We identified a novel CRC-related lncRNA, MCF2L-AS1, which is distinctly highly expressed in CRC. Its diagnostic value for CRC patients was also demonstrated. Clinical assays revealed that high MCF2L-AS1 expression is associated with advanced stages, positive metastasis and the poor prognosis of CRC patients. Multivariate assays confirmed that MCF2L-AS1 expression is an independent poor prognostic factor for both 5-year overall survival and 5-year disease-free survival of CRC patients. Functionally, we confirmed that knockdown of MCF2L-AS1 distinctly suppresses the proliferation, migration and invasion of CRC cells and also promotes apoptosis. Mechanistic investigation showed that MCF2L-AS1 functions as an endogenous sponge for miR-874-3p to increase the expression of CCNE1. CONCLUSIONS: Our findings identified a novel CRC-related lncRNA, MCF2L-AS1, which may be used as a potential diagnostic and prognostic biomarker for CRC patients. In addition, the newly identified MCF2L-AS1/miR-874-3p/CCNE1 axis can modulate the initiation and progression of CRC.

Changes in levels of coagulation parameters in different trimesters among Chinese pregnant women.

BACKGROUND: This article is to explore changes in levels of coagulation parameters in different trimesters among healthy pregnant women in China. METHODS: A total of 760 eligible women were enrolled (first-trimester group: n = 183, second-trimester group: n = 183, third-trimester group: n = 263, non-pregnant group: n = 131). Seven parameters including prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), fibrinogen (FIB), D-dimer (DD), fibrinogen degradation products (FDP), and antithrombin III (ATIII), of all participants were collected. The non-parametric 2.5th-97.5th percentiles reference intervals were calculated for each parameter. RESULTS: The reference intervals for FIB, PT, APTT, TT, FDP, DD, and ATIII at first trimester were 2.11-4.32 g/L, 10.90-13.85 s, 24.60-39.28 s, 12.95-15.88 s, 0.04-2.55 µg/mL, 0.03-1.15 µg/mL, and 75.57%-125.31%, respectively. The reference intervals at second trimester were 2.31-4.77 g/L, 9.70-12.64 s, 24.16-35.43 s, 12.95-15.88 s, 0.15-7.40 µg/mL, 0.08-2.13 µg/mL, and 74.35%-119.28%, respectively. For the third-trimester, the intervals were 2.39-4.96 g/L, 9.20-11.95 s, 23.90-35.51 s, 13.41-18.00 s, 0.55-13.43 µg/mL, 0.15-3.60 µg/mL, and 71.61%-118.29%, respectively. The third-trimester group showed decreased PT, APTT, and ATIII and increased FIB, TT, DD and FDP as compared with the other groups. CONCLUSION: In this study, level changes of coagulation parameters in different trimesters were observed. And the ranges for coagulation parameters were presented, which may provide some reference for clinicians to more accurately monitor the coagulation and fibrinolytic system in pregnant women.

Small RNA sequencing reveals a novel tsRNA-06018 playing an important role during adipogenic differentiation of hMSCs.

Transfer RNA-derived small RNAs (tsRNAs), a novel type of non-coding RNA derivative, are able to regulate a wide range of biological processes. What role these tsRNAs play in the regulation of human bone marrow mesenchymal stem cell (hMSCs) adipogenic differentiation remains uncertain. We induced the adipogenic differentiation of human bone marrow mesenchymal cells (hMSCs) and then performed small RNA transcriptomic sequencing, leading us to identify tsRNA-06018 as a target of interest based upon resultant the tsRNA expression profiles. When tsRNA-06018 was knocked down, this led to the inhibition of adipogenesis and a decrease in adipogenic marker expression. When STC2 was overexpressed, this impaired the adipogenic differentiation of these cells. We further used luciferase reporter assays to confirm that tsRNA-06018 directly binds the 3'-untranslated region (3'-UTR) of STC2. In addition, we determined that both knocking down tsRNA-06018 and overexpressing STC2 increased extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation within cells. We also assessed that the adipogenic differentiation of hMSCs in which tsRNA-06018 was knocked down was further enhanced upon the addition of the ERK1/2 inhibitor U0126 as compared tsRNA-06018 knockdown alone. Taken together, using small RNA sequencing we profiled tsRNAs in hMSCs during the process of adipogenesis, leading us to identify tsRNA-06018 as a novel regulator of this differentiation process. This tsRNA was able to regulate adipogenic differentiation by targeting STC2 via the ERK1/2 signalling pathway.

The factors related to failure of Enhanced Recovery after Surgery (ERAS) in colon cancer surgery.

PURPOSE: Enhanced Recovery after Surgery has been proven effective for patients with gastrointestinal cancer. But radical enhanced recovery could also lead to adverse clinical outcomes. Compared with reports on the estimation of successful implementation of enhanced recovery, studies on risk factors of enhanced recovery failure are still lacking. METHODS: A retrospective analysis was carried out on 102 patients in ERAS who underwent elective colon cancer surgery. This study included 102 patients with colon cancer between 2015 and 2019, defining enhanced recovery failure as postoperative length of stay over 10 days, stay in ICU over 24 h after surgery, reoperation, death, or unplanned readmission within 30 days after surgery. Univariate and multivariate analyses were performed to explore potential risk factors of failure. RESULTS: Aged ≥ 75, open operation, number of drainage tube over 1, re-urethral catheterization, and Clavien-Dindo grade over 2 were associated with ERAS failure, according to univariate analysis. Multivariate analysis showed that age ≥ 75 [OR 7.231; P = 0.009]; open operation (OR 3.599; P = 0.021); and number of drainage tube over 1 (OR 3.202; P = 0.020) were independent risk factors for ERAS failure. CONCLUSIONS: We found age ≥ 75, open operation, and number of drainage tube over 1 are independent risk factors associated with ERAS failure after colon cancer surgery.

5-Substituted-N-pyridazinylbenzamides as potent and selective LRRK2 inhibitors: Improved brain unbound fraction enables efficacy.

We describe the discovery and optimization of 5-substituted-N-pyridazinylbenzamide derivatives as potent and selective LRRK2 inhibitors. Extensive SAR studies led to the identification of compounds 18 and 23, which demonstrated good in vitro pharmacokinetic profile and excellent selectivity over 140 other kinases. Both compounds demonstrated high unbound fractions in both blood and brain. Compound 18 proved to be brain penetrant, and the high unbound fraction of compound 18 in brain enabled its in vivo efficacy in CNS, wherein a significant inhibition of LRRK2 Ser935 phosphorylation was observed in rat brain following intravenous infusion at 5 mg/kg/h.

Discovery of 4-ethoxy-7H-pyrrolo[2,3-d]pyrimidin-2-amines as potent, selective and orally bioavailable LRRK2 inhibitors.

Inhibition of LRRK2 kinase activity with small molecules has emerged as a potential novel therapeutic treatment for Parkinson's disease. Herein we disclose the discovery of a 4-ethoxy-7H-pyrrolo[2,3-d]pyrimidin-2-amine series as potent LRRK2 inhibitors identified through a kinase-focused set screening. Optimization of the physicochemical properties and kinase selectivity led to the discovery of compound 7, which exhibited potent in vitro inhibition of LRRK2 kinase activity, good physicochemical properties and kinase selectivity across the kinome. Moreover, compound 7 was able to penetrate into the CNS, and in vivo pharmacology studies revealed significant inhibition of Ser935 phosphorylation in the brain of both rats (30 and 100 mg/kg) and mice (45 mg/kg) following oral administration.

Discovery of 5-substituent-N-arylbenzamide derivatives as potent, selective and orally bioavailable LRRK2 inhibitors.

Leucine-rich repeat kinase 2 (LRRK2) has been suggested as a potential therapeutic target for Parkinson's disease. Herein we report the discovery of 5-substituent-N-arylbenzamide derivatives as novel LRRK2 inhibitors. Extensive SAR study led to the discovery of compounds 8e, which demonstrated potent LRRK2 inhibition activity, high selectivity across the kinome, good brain exposure, and high oral bioavailability.

One-step solvent extraction followed by liquid chromatography-atmospheric pressure photoionization tandem mass spectrometry for the determination of polycyclic aromatic hydrocarbons in edible oils.

A method for rapid analysis of 16 polycyclic aromatic hydrocarbons (PAHs) in edible oils has been developed on the basis of a simplified solvent extraction and liquid chromatography-atmospheric pressure photoionization tandem mass spectrometry performed in multiple reaction monitoring mode. The briefness of the experimental procedure, the use of milliliters of acetonitrile for extraction without any further cleanup process, the short analysis time, and the excellent sensitivity and selectivity demonstrated the advantages of this practical and environmentally friendly method. All the analytes exhibited satisfactory recoveries at three spiking levels (the recoveries ranged from 77.8 to 106.4%), and the relative standard deviations were lower than 10%. The limits of quantitation of this method for the 16 PAHs were in the range of 0.02-0.43 µg/kg. The validated method was successfully applied for the determination of PAHs in coconut oil reference material (BCR-458) and real edible oil samples. The results suggested that a large-scale investigation of the concentration of PAHs in vegetable oils in China is required.

Enhancing Persistent Luminescence through Synergy between Optimal Electron Traps and Dye Sensitization.

Due to their unique afterglow ability, long-wavelength-light rechargeable persistent luminescence (PersL) nanoparticles (PLNPs) have been emerging as an important category of imaging probes. Among them, ZnGa2O4:0.6% Cr3+ (ZGC) PLNPs have gained widespread recognition due to the ease of synthesis and uniform morphology. Unfortunately, the limited absorption arising from the low molar extinction coefficient of Cr3+ results in relatively low afterglow intensity and rapid decay after long-wavelength LED light irradiation. Herein, we discovered a strategy that boosting dye-sensitization performance was able to effectively amplify the PersL signal under white LED light. Specifically, Dil served as a highly efficient sensitizer for Cr3+, promoting the absorption of the excitation light. By adjusting the Pr dopant concentrations, ZGCP0.5 PLNPs with optimal trap densities were obtained, which showed the highest PersL intensity and dye-sensitized performance. Strikingly, ZGCP0.5-Dil PLNPs exhibited a 24.3-fold enhancement in intensity and a 2-fold prolongation of decay time over bare ZGC PLNPs through the synergy effect of optimal electron traps and dye sensitization. Photostable ZGCP0.5-Dil PLNPs enabled imaging of the HepG2 tumor and effectively guided tumor surgical resection verified by the H&E staining analysis. This strategy could be a significant reference in other dye-sensitization PLNPs to enhance longer-wavelength rechargeable PersL.

The extract of an herbal medicine Chebulae fructus inhibits hepatocellular carcinoma by suppressing the Apelin/APJ system.

Introduction: Hepatocellular carcinoma (HCC) has been a highly common and pathological disease worldwide, while current therapeutic regimens have limitations. Chebulae Fructus, a common herbal medicine in Asia, has been documented to exert potential therapeutic effects on HCC in ancient medicine clinical practice. However, the molecular mechanism underlying its inhibitory effects on HCC requires further investigation. Methods: In this study, the anti-HCC effect of the aqueous extract of Chebulae Fructus (CFE) on human HCC and its underlying mechanism were evaluated. Assays including CCK8, EdU staining, crystal violet staining, cell clone formation, flow cytometry, wound healing, and transwell were used in vitro. The cell-derived xenograft (CDX) and patient-derived xenograft (PDX) models were used in vivo. Transcriptomics analysis, qRT-PCR, ELISA, IHC staining, and Western blotting were employed to determine the mechanism of action of CFE. Results: The results demonstrate that CFE effectively suppressed the proliferation and activity of HepG2 and PLC/PRF/5 HCC cells. CFE also induced apoptosis, and suppressed the migration and invasion abilities of these cells. Furthermore, CFE exhibited inhibitory effects on tumor growth in both H22 and PLC/PRF/5 mouse models, as well as in an HCC PDX model which is derived from patient tumor samples. Moreover, it was identified that CFE treatment specifically suppressed the Apelin/APJ system in HCC cells and tumor tissues. To investigate the role of the Apelin/APJ system in mediating the effects of CFE treatment, an APJ overexpressed cell model is established. Interestingly, it was found that the overexpression of APJ significantly diminished the inhibitory effects of CFE on HCC in vitro. Discussion: Collectively, this study provides compelling evidence that CFE exerts significant anti-HCC effects in cell and animal models. Moreover, our findings suggest that the Apelin/APJ system may play a vital role in the therapeutic effects of CFE against HCC.

Small molecule inhibition of phosphatidylinositol-3,4,5-triphosphate (PIP3) binding to pleckstrin homology domains.

The PI3-kinase (PI3K) pathway regulates many cellular processes, especially cell metabolism, cell survival, and apoptosis. Phosphatidylinositol-3,4,5-trisphosphate (PIP3), the product of PI3K activity and a key signaling molecule, acts by recruiting pleckstrin-homology (PH) domain-containing proteins to cell membranes. Here, we describe a new structural class of nonphosphoinositide small molecule antagonists (PITenins, PITs) of PIP3-PH domain interactions (IC(50) ranges from 13.4 to 31 µM in PIP3/Akt PH domain binding assay). PITs inhibit interactions of a number of PIP3-binding PH domains, including those of Akt and PDK1, without affecting several PIP2-selective PH domains. As a result, PITs suppress the PI3K-PDK1-Akt pathway and trigger metabolic stress and apoptosis. A PIT-1 analog displayed significant antitumor activity in vivo, including inhibition of tumor growth and induction of apoptosis. Overall, our studies demonstrate the feasibility of developing specific small molecule antagonists of PIP3 signaling.

Sensitization of colon cancer cells to cisplatin by Fbxw7 via negative regulation of the Nox1-mTOR pathway.

Colorectal cancer (CRC) is a human malignancy which associates with high mortality rate and poor prognosis. Despite the initial effectiveness in clinical applications of chemotherapeutic agents, a fraction of patients develops chemoresistance. Fbxw7 is an F-box protein serving as a substrate recognition subunit of E3 ubiquitin ligase, leading to degradation of various oncoproteins. In this study, Fbxw7 was significantly downregulated in CRC tumors as well as CRC cells. Fbxw7 suppressed CRC cell proliferation and migration. Moreover, we observed Fbxw7 was positively associated with cisplatin sensitivity. Fbxw7 was significantly downregulated in cisplatin resistant CRC cells. Overexpression of Fbxw7 effectively increased the cisplatin sensitivity of cisplatin resistant CRC cells. Co-immunoprecipitation and GST pull-down assays showed Fbxw7 bond with Nox1 which was a superoxide-generating NADPH oxidase and showed oncogenic roles in colon cancer cells. Interestingly, Fbxw7 downregulated Nox1 through binding it to degrade Nox1 protein. We demonstrated that Fbxw7 negatively regulated mTOR activity through downregulation of Nox1. Finally, overexpression of Fbxw7 effectively increased the cisplatin sensitivity of CRC cells. This process could be further overturned by Nox1 restoration in Fbxw7-overexpressing colon cancer cells. In summary, these results unveiled that Fbxw7 targeted Nox1 for degradation, resulting in blocking the downstream Nox1-mTORC1 signaling to sensitize CRC cells to cisplatin. Our study potentiates that targeting the Fbxw7-Nox1-mTOR pathway could be an effective approach to overcome chemoresistance of colon cancer cells.

Light-sheet laser speckle imaging for cilia motility assessment.

Mucociliary clearance is an important innate defense mechanism predominantly mediated by ciliated cells in the upper respiratory tract. Ciliary motility on the respiratory epithelium surface and mucus pathogen trapping assist in maintaining healthy airways. Optical imaging methods have been used to obtain several indicators for assessing ciliary movement. Light-sheet laser speckle imaging (LSH-LSI) is a label-free and non-invasive optical technique for three-dimensional and quantitative mapping of velocities of microscopic scatterers. Here, we propose to use an inverted LSH-LSI platform to study cilia motility. We have experimentally confirmed that LSH-LSI can reliably measure the ciliary beating frequency and has the potential to provide many additional quantitative indicators for characterizing the ciliary beating pattern without labeling. For example, the asymmetry between the power stroke and the recovery stroke is apparent in the local velocity waveform. PIV (particle imaging velocimetry) analysis of laser speckle data could determine the cilia motion directions in different phases.

Overexpression of TWF1 promotes lung adenocarcinoma progression and is associated with poor prognosis in cancer patients through the MMP1 signaling pathway.

Background: It has been reported that twinfilin actin binding protein 1 (TWF1) is associated with the progression of breast and pancreatic cancers. However, the roles and mechanisms of TWF1 in lung adenocarcinoma (LUAD) have not been reported. Methods: The expression levels of TWF1 in LUAD and normal tissues were analyzed using The Cancer Genome Atlas (TCGA) database, and validation was carried out with 12 clinical samples. The relationship between TWF1 expression and LUAD patients' clinical indices and immunity was investigated. Cell Counting Kit-8 (CCK-8) and migration and invasion assays were employed to explore the effects of downregulated TWF1 on LUAD cell proliferation and metastasis. Results: TWF1 was upregulated in LUAD tissues, and upregulated TWF1 was correlated with the tumor (T) stage, node (N) stage, clinical classification, overall survival (OS), and progression-free interval (PFI) of LUAD patients. Moreover, the Cox regression analysis showed that TWF1 overexpression was an independent risk factor for the poor prognosis of LUAD patients. TWF1 expression was associated with tumor immune infiltration (such as dendritic cells resting, eosinophils, macrophages M0, and others), drug sensitivity (such as A-770041, Bleomycin, and BEZ235), tumor mutation burden (TMB), and sensitivity to immunotherapy. In the cell model, TWF1 expression interference significantly prohibited LUAD cell proliferation, migration, and invasion, which might be relevant to aberrant MMP1 protein downregulation. Conclusions: TWF1 overexpression was correlated with poor prognoses and immune status of LUAD patients. Inhibited TWF1 expression delayed the growth and migration of cancer cells by downregulating MMP protein, implying that TWF1 is a promising biomarker for the prognoses of LUAD patients.

Corrigendum: Effects of a pair programming educational robot-based approach on students' interdisciplinary learning of computational thinking and language learning.

[This corrects the article DOI: 10.3389/fpsyg.2022.888215.].

Myeloperoxidase-antineutrophil cytoplasmic antibody-associated vasculitis with headache and kidney involvement at presentation and with arthralgia at relapse: A case report.

BACKGROUND: Patients with proteinase 3-antineutrophil cytoplasmic antibody associated vasculitis (AAV) experience different manifestations at the initial onset and relapse. However, such cases of different initial and relapse manifestations have not been reported in myeloperoxidase (MPO)-AAV patients. CASE SUMMARY: A 52-year-old woman was admitted to our hospital because of headache. Laboratory findings indicated nephrotic range proteinuria and microscopic hematuria, serum creatinine of 243 µmol/L, anti-MPO antibody titer of > 400 RU/mL, and positive perinuclearantineutrophil cytoplasmic antibody. Renal biopsy showed pauci-immune crescentic glomerulonephritis. The cerebrospinal fluid examination and brain magnetic resonance imaging did not show any abnormality. Therefore, MPO-AAV was diagnosed. Corticosteroids, plasmapheresis, and cyclophosphamide as induction therapy and mycophenolate mofetil (MMF) as maintenance therapy were administered. The patient's headache disappeared; serum creatinine returned to normal; complete remission of microscopic hematuria and proteinuria was observed. Anti-MPO antibody titer reached normal limits after immunosuppressive treatment. Twenty-five months after stopping the immunosuppressive treatment, the patient relapsed with arthralgia, without neurological or renal involvement. The patient's arthralgia improved after treatment with prednisone and MMF. CONCLUSION: We have reported a rare case of MPO-AAV who initially presented with headache and kidney involvement. However, relapse presented with only arthralgia, which was completely different from the initial manifestations. This case suggests that AAV relapse should be highly suspected in MPO-AAV patients after remission, when clinical manifestations at relapse are different from those at onset. Prednisone and MMF may provide a good choice for refractory arthralgia during relapse in MPO-AAV patients.