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JOURNAL OF PHARMACEUTICAL AND BIOMEDICAL ANALYSIS · 2025 · IF 3.1

Integrating 16S rDNA sequencing analysis and targeted metabolomics to explore the mechanism of Xiexin Tang in treating atherosclerosis mice induced by high-fat diet

Junling Li,Qianru Gao,Hongtao Liu,Songlin Liu,Yanchun Wang,Xiongjie Sun,Junping Zheng,Huabing Yang,Baifei Hu

Xiexin Tang (XXT) is a classic Chinese medicine formula that can be used to treat Atherosclerosis (AS). This study aimed to investigate the mechanism by which XXT regulated AS lipid levels. Firstly, the mixture components of XXT were analyzed by High-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). Then, the AS model based on Apolipoprotein E knockout (ApoE -/- ) mice was established. Cytokines related to lipid metabolism and bile acid metabolism were detected by Quantitative Real-time PCR (qRT-PCR). 16S rDNA gene sequencing was performed to analyze differential bacterial populations, and the mechanism of XXT regulation of bile acids affecting lipid metabolism was further explored by targeted metabolomics. Further, antibiotic-treated mice were used to investigate the role of gut microbiota in the anti-AS effect of XXT. The results showed that XXT attenuated the lipid levels and reversed the abnormal elevation of cytokines, such as hepatic lipid metabolism and inflammatory reaction in AS mice. XXT also repaired the gut barrier damage and reversed gut microbiota disorders in AS mice. Furthermore, the metabolic levels of bile acids were reshaped by XXT. Whereas, in the absence of gut microbiota, XXT failed to attenuate lipid levels and inhibit the expression of cytokines related to inflammation and bile acid metabolism in AS mice and failed to play a role in ultimately treating AS. In conclusion, XXT could effectively inhibit the inflammatory reaction and lipid accumulation in AS mice, and this effect was closely related to its remodeling of gut microbiota to regulate bile acid metabolism.

✓ 已验证 产品关联 DOI PubMed 高影响因子
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OPTICS AND LASER TECHNOLOGY · 2026 · IF 5.2

Highly sensitive vancomycin detection using a fiber-optic sensor with AuNPs/MWCNTs/DNA aptamer synergistic modification

Like Li,Shunye Huang,Yi Li,Xiaoman Chen,Qiwei Li,Hui Tang,Xuqiang Wu,Yong Zhao

Due to its narrow treatment window, the vancomycin concentration in the patient’s body needs to be monitored regularly to guide dose optimization and ensure safety and efficacy. Here, we developed a fiber-optic surface plasmon resonance (SPR) vancomycin sensor based on gold nanoparticles (AuNPs)/multiwalled carbon nanotubes (MWCNTs)/DNA aptamer synergistic modification. AuNPs can effectively enhance the local electromagnetic field and plasmon resonance effects, while MWCNTs have a strong electronic conductivity and a high specific surface area. The synergistic effect of the two can achieve dual amplification of the SPR signal, thereby improving the sensitivity. Vancomycin aptamer can specifically capture vancomycin molecules and induce spatial conformational changes, thereby increasing the effective refractive index. Experimental results confirmed that within 30 μM–400 μM, the sensitivity of vancomycin detection is as high as 0.0527 nm/μM, and the detection limit is 18.11 μM. Moreover, the vancomycin sensor exhibits excellent stability and specificity. The vancomycin sensor is low-cost, easy to use, and has the potential to be applied for rapid and accurate determination of vancomycin in clinical settings.

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JOURNAL OF ETHNOPHARMACOLOGY · 2026 · IF 6.8

Da-Jian-Zhong decoction restores the gut-brain balance in diarrhea-predominant irritable bowel syndrome rats via gut microbiota-bile acid axis

Huan-qing Gao,Ning Zhang,Ge-ning Li,Li Wen,Yao Li,Min Li,Tai-wei Dong,Lian Zhong,Da-neng Wei,Meng-meng Zhang,Li Ou

Ethnopharmacological relevance Da- Jian-Zhong decoction (DJZD), a Chinese medicinal formula, exhibits therapeutic effects in the clinical management of diarrhea-predominant irritable bowel syndrome (IBS-D). Accumulating studies have demonstrated that DJZD can regulate the gut-brain balance in IBS-D model rats; however, its underlying molecular mechanism remains unclear. Aim of the study To explore the potential mechanism by which DJZD restores the gut-brain axis in IBS-D model rats. Materials and methods Firstly, the therapeutic effects of DJZD in IBS-D model rats were evaluated based on the Bristol stool scale, abdominal withdrawal reflex (AWR) score, open field test (OFT) behavior, intestinal barrier integrity, and brain-gut peptide levels. Moreover, alterations in gut microbiota was detected using sequencing of the whole microbial genome. Subsequently, fecal microbiota transplantation (FMT) was performed to explore whether the regulatory effect of DJZD on the gut-brain axis against IBS-D was dependent on gut microbiota. The UHPLC-QTRAP-MS/MS was utilized to analyze bile acids (BAs) profiles and identify gut microbiota-derived BAs metabolites responsible for the beneficial effects of DJZD. Finally, the role of BAs metabolites in restoring the gut-brain axis was further verified using the IBS-D model rats. Results Treatment with DJZD not only decreased AWR score, improved stool score and intestinal barrier integrity, but also enhanced sucrose preference and changed OFT performance of IBS-D rats. Meanwhile, DJZD normalized the levels of 5-hydroxytryptamine (5-HT) and substance P (SP) in both the colon and hippocampus. Fecal microbiota harvested from DJZD-treated rats also reversed these IBS-D-associated pathological manifestations. Moreover, DJZD notably elevated the levels of secondary BAs (SBAs) in colonic contents of IBS-D rats, particularly norchenodeoxycholic acid (NorDCA), lithocholic acid (LCA), deoxycholic acid (DCA), and 3β-ursodeoxycholic acid (3β-UDCA). The elevated SBAs were positively correlated with the relative abundances of Akkermansia sp., Ruminococcus sp., and Clostridium sp. This could be attributed to the ability of these bacteria to produce bile salt hydrolases (BSH) and 7α-hydroxysteroid dehydrogenases (7α-HSDH). Additionally, administration of an LCA and DCA mixture was found to improve intestinal and brain dysfunction and restored abnormal 5-HT and SP levels in IBS-D rats. Conclusion DJZD restores gut-brain balance in IBS-D rats by regulating gut microbiota-bile acid axis, which provides a promising therapeutic strategy for IBS-D via targeting bile acid metabolites and intestinal bacteria.

✓ 已验证 产品关联 DOI PubMed 高影响因子
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Advanced Science · 2026 · IF 14.1

Bifidobacterium Pseudolongum‐Derived Inosine Mitigates Polystyrene Nanoplastics‐Induced Hepatic Injury by Inhibiting the Polarization of M1 Macrophages

Kaikai Zhang,Yuchuan Chen,Jiayuan Wan,Jianzheng Yang,Lijian Chen,Qingyuan Li,Anding Zhou,Nian Zhou,Jiuyang Ding,Qi Wang,Jian Sun

Nanoplastics (NPs) exposure can cause severe hepatic injuries. Gut microbiota is considered a contributing factor to multiple hepatic injuries. However, its role in NPs‐induced hepatic injuries remains unclear, and microbial intervention strategies are required. Our results reveal that oral exposure to polystyrene NPs reduces gut probiotic Bifidobacterium pseudolongum ( B.p ) and its metabolite inosine. Gut microbiota from NPs‐administered mice partially reproduces NPs‐related impairment of gut homeostasis and hepatic injury in recipient mice. Moreover, B.p colonization improves NPs‐induced gut homeostasis impairment and hepatic injury, and its protective effects are reproduced by supplementation with inosine. Mechanically, B.p colonization increases hepatic level of inosine and subsequently normalizes the expression of its target A2AR. Meanwhile, increased inosine inhibits the miR155/SOCS1/NF‐κB pathway and represses NPs‐induced M1 macrophage polarization. CGS21680 , an agonist of A2AR, effectively represses lipopolysaccharide (LPS)‐induced M1 macrophage polarization and inhibits the miR155/SOCS1/NF‐κB pathway in vitro. Further, miR155 knockout inhibits NPs‐induced M1 macrophage polarization, but does not influence the suppression of NPs on A2AR. These findings suggest that B.p ‐derived inosine can repress NPs‐induced M1 macrophages polarization by inhibiting the miR155/SOCS1/NF‐κB pathway via targeting A2AR. Altogether, this study further clarifies the role of gut microbiota in NPs‐induced hepatic injury and provides a potential microbial therapeutic strategy. Probiotic B.p colonization elevated gut‐derived inosine level in the liver, while elevated inosine activated A2AR and subsequently blocked NPs‐induced polarization of M1 macrophages by repressing the miR155/SOCS1/NF‐κB pathway. This reduced the release of inflammatory cytokines and thereby, mitigated NPs‐induced hepatic injury.

✓ 已验证 产品关联 DOI PubMed 高影响因子
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Food Science & Nutrition · 2026 ·Vol. 14 ·期 7 ·e72122 · IF 5

Microbiota-Targeted Chitooligosaccharides Intervention Restores Glucose Homeostasis After Islet Cell Transplantation in Rapamycin-Treated Mice

Kunlin Chang,Duowen He,Junfeng Dong,Yayu Zhang,Shuxin Deng,Mengyao Zhao,Jiayang Jin,Xiaoguo Ji,Hao Yin,Liming Zhao

Islet cell transplantation (ICT) is an effective treatment for diabetes mellitus, but postoperative islet function recovery and inflammation are closely linked to immunosuppressants. Using multi-omics and fecal microbiota transplantation (FMT) in human microbiota-associated (HMA) mice, this study explored rapamycin-induced gut dysbiosis and its impacts on islet function and inflammation post-ICT. ICT significantly altered the gut microbiota of type 2 diabetes mellitus (T2DM) patients, and FMT from these patients to antibiotic-treated mice recapitulated metabolic disorders in the mice. These disorders included hyperglycemia, hepatic and pancreatic injury, and impaired intestinal barrier. Rapamycin decreased beneficial bacteria ( Akkermansia , Faecalibacterium ) and enriched Desulfovibrio in HMA-T2DM mice. Targeted microbial modulation by chitooligosaccharides (COS) ameliorated rapamycin-induced deficits in insulin and C-peptide secretion, as well as elevated glycated hemoglobin levels. COS also significantly reduced serum inflammatory markers IP-10 and MCP-1, while upregulating colonic barrier proteins ( Muc2 , Occludin ) in HMA-T2DM-ICT mice. COS additionally mitigated postoperative hyperglycemia via the PI3K/AKT/GSK3β/FOXO1 signaling pathway. This study identified COS as a microbiota-targeted adjunctive strategy to improve metabolic recovery and islet function under post-transplant immunosuppression.

CAS / MDL: 1404-90-6
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PLoS One · 2026 ·Vol. 21 ·期 7 ·e0351316 · IF 2.8

An exercise-associated gut microbiota signature enhances endurance performance: A study combining a human cohort and a mice FMT model

Xiongbao Zhang,Yating Fu,Jiahui Chen,Hao Shen,Yumeng Du,Jun Wu,Hongjing Lai,Yu Liu,Jingbo Chen,Xiaomei Hou,Wenjun Chang,Xuefei Hu

Background The gut microbiota is closely related to exercise, but the interrelationship between the two remains elusive. In this study, we aimed to explore differences in the gut microbiota between young adults with exercise and sedentary lifestyles. In addition, we evaluated the effects of gut microbiota from these different lifestyle populations on endurance exercise capacity. Methods The exercise status and nutritional characteristics of young adults were evaluated by PARS-3 and food frequency questionnaires. The gut microbiota of young adults from exercise and sedentary lifestyle groups was analyzed by 16S rRNA analysis. Subsequently, we performed fecal bacteria transplantation (FMT) from the human donors into mice and evaluated the effects on their endurance exercise capacity. Results The exercise group exhibited significantly higher gut microbiota diversity compared to the sedentary group. Several beneficial bacteria, including Veillonella, Faecalibacterium, and Bacteroides, were enriched in the exercise group. The FMT experiment confirmed that mice receiving microbiota from the exercise group showed significantly improved endurance exercise capacity. Conclusion Young people who exercise regularly possess a more diverse gut microbiota enriched with beneficial bacteria. This exercise-associated microbiota has the potential to directly improve exercise capacity.

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Natural Products and Bioprospecting · 2026 ·Vol. 16 ·期 1 ·76 · IF 5.8

Huanglian-Wendan Decoction alleviates DSS-induced colitis by modulating the gut microbiota and protecting against intestinal injury via suppression of colonic apoptosis and endoplasmic reticulum stress

Li Liang,Zhan Xinyi,Ullah Hidayat,Guo Wenxian,Gui Ping,Peng Weijie,Mei Quanxi,Dai Weibo,Duan Yuting,Yuan Xia,Hu Xianjing

Inflammatory bowel disease (IBD) is a chronic disorder characterized by recurrent intestinal inflammation and gut microbiota dysbiosis. Huanglian-Wendan Decoction (HLWDD) has been clinically used for IBD treatment; however, its underlying mechanisms remain unclear. In this study, a dextran sulfate sodium (DSS, 2.25%)-induced IBD mouse model was established to evaluate the therapeutic effects of HLWDD. The protective mechanisms were investigated in colon tissues of DSS-induced mice using ELISA, immunoblotting, histological, and immunohistochemical analyses. In addition, the impact of HLWDD on gut microbiota dysbiosis was analyzed using 16S rRNA sequencing. Antibiotic treatment was applied before DSS administration to deplete gut microbiota and verify the role of microbial modulation. Furthermore, the phytochemical constituents of HLWDD were characterized using liquid chromatography–quadrupole time-of-flight tandem mass spectrometry (LC-QTOF-MS/MS). The results demonstrated that HLWDD markedly alleviated DSS-induced colitis, as evidenced by reduced body weight loss, rectal bleeding, colon shortening, and disease activity index (DAI) scores. Mechanistically, HLWDD suppressed inflammatory responses in colon tissues by inhibiting the TLR4/MyD88/NF-κB and IL-6/JAK2/STAT3 signaling pathways, while enhancing epithelial barrier integrity through upregulation of ZO-1, Occludin, Claudin-1, and Mucin-2. In addition, HLWDD attenuated endoplasmic reticulum stress (ERS) and apoptosis by downregulating CHOP, phospho-eIF2α, cleaved caspase-3, and Bax, while increasing Bcl-2 expression in colonic tissues. Microbiota analysis revealed an increased abundance of beneficial bacterial genera such as Akkermansia and Escherichia-Shigella –related commensals, along with enrichment of beneficial bacterial families including Ruminococcaceae , Lachnospiraceae , and Verrucomicrobiaceae , whereas potentially harmful taxa such as Escherichia and Paraprevotella were reduced. HLWDD also increased the production of short-chain fatty acids (SCFAs), including acetate, butyrate, and isobutyrate, thereby promoting intestinal homeostasis. Importantly, the protective effects of HLWDD were largely abolished following antibiotic-mediated gut microbiota depletion, confirming the essential role of microbial modulation in its therapeutic action. Collectively, these findings suggest that HLWDD ameliorates IBD by regulating gut microbiota composition and function, thereby inhibiting colonic ER stress and apoptosis and restoring intestinal barrier integrity. This study provides mechanistic evidence supporting the potential clinical application of HLWDD as a novel therapeutic strategy for IBD. Graphical

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Cell Host & Microbe · 2026 · IF 23.2

Commensal enteric virome regulates intestinal carbohydrate digestion and absorption

Fengqing Lin,Lianglan Li,Yuanpeng He,Shujie Xu,Qiufen Mo,Wangsen Cao,Aikun Fu,Weiqin Li

The enteric microbiome and nutrient sensing within the small intestine play critical roles in maintaining host metabolic homeostasis. Although various bacteria and some fungi have established functions in nutrient metabolism, the role of the enteric virome remains poorly understood. Here, we demonstrate that the enteric virome significantly influences carbohydrate digestion and absorption independently of the bacteriome. Furthermore, the virome elicits distinct responses across different intestinal cell types. Specifically, it activates programs for carbohydrate digestion and absorption in intestinal epithelial cells while simultaneously stimulating antigen-presenting cells―Th17 cells―to produce interleukin-22, a cytokine that curbs excessive carbohydrate uptake. The virome’s effect on carbohydrate digestion and absorption—whether suppressive or stimulatory—depends on the presence or absence of immune surveillance. This intricate interplay between metabolic and immune pathways establishes the enteric virome as a pivotal regulator of metabolism and reveals the virome’s intrinsic capacity to autonomously modulate vertebrate intestinal physiology.

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ANALYTICAL AND BIOANALYTICAL CHEMISTRY · 2026 · IF 4.1

A CQDs-doped europium-DPA framework for fluorescence and colorimetric dual-mode sensing of amoxicillin and ciprofloxacin

Yi Jintao,Fu Nani,Zhong Wenhui,Liu Xia,Zhou Anqi,Li Xun

Amoxicillin (AMO), a penicillin antibiotic, and ciprofloxacin (CIP), a quinolone antibiotic, are widely used to combat bacterial infections and are frequently co-administered to enhance therapeutic efficacy. However, improper use of AMO and CIP may lead to antibiotic residues in the environment, posing serious threats to human health. The visual detection of AMO and CIP remains significant challenges. Herein, the Eu-DPA@CQDs was used for the dual-mode detection of AMO and CIP, which was synthesized by CQDs doped in europium-DPA metal-organic framework. In the colorimetric mode, the catalase-mimicking Eu-DPA@CQDs oxidized TMB to blue oxTMB. Upon addition of AMO, the oxTMB was reduced, causing color fading. Subsequent introduction of CIP restored nanozyme activity, regenerating the blue signal and enabling dual-analyte antibiotic detection. In the fluorescence mode, the Eu-DPA@CQDs probe exhibited dual emission at 440 nm and 613 nm. Upon AMO addition, the fluorescence at both wavelengths was quenched, accompanied by a color change from red to purple. In the presence of CIP, the emission at 440 nm increased and redshifted to 490 nm, while the signal at 613 nm was quenched, resulting in a multicolor transition from red to cyan. The Eu-DPA@CQDs sensor enabled rapid and dual-mode detection of AMO and CIP. The colorimetric method exhibited wide linear ranges of 0.005–25 μM for AMO and 0.007–4.25 μM for CIP, with detection limits of 1.67 nM and 3.75 nM, respectively. A visible color transition from dark blue to colorless was observed with increasing AMO concentration, while the addition of CIP reversed the signal back to dark blue. Similarly, the fluorescence detection achieved wide linear ranges from 0.005 to 30 μM for AMO and 0.005 to 15 μM for CIP, with detection limits as low as 4.74 nM and 3.11 nM, respectively, also within only 1 min. As the concentration of AMO increased, the color shifted from red to purple. In contrast, increasing CIP concentration induced a color transition from red to cyan. These color transitions were both clearly visible to the naked eye. The sensor demonstrated excellent selectivity and anti-interference capability, providing a reliable platform for accurate, sensitive, and quantitative determination of both antibiotics in real samples. Graphical abstract

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BIOORGANIC CHEMISTRY · 2026 · IF 5.1

Rational β-turn engineering of a disulfide-free β-hairpin-like antimicrobial peptide W2PG with enhanced stability, selectivity, and in vivo efficacy

Meng Liu,Peng Jiang,Binghui Ruan,Yunfei Cui,Junjie Zhang,Yuxiu Ye,Dongting Zhangsun,Sulan Luo,Yong Wu

Antimicrobial resistance (AMR) is an increasing global concern, while the development of new antibiotics remains limited. Antimicrobial peptides (AMPs) offer an alternative due to their broad-spectrum and membrane-targeting features, but their translation is restricted by instability and cytotoxicity. Here, we describe a β-turn engineering strategy that incorporates a Pro-Gly motif and aromatic residues to create a short, disulfide-free β-hairpin-like AMP (W2PG). W2PG showed broad-spectrum activity (MIC 4–8 μM) with low hemolysis and cytotoxicity, along with improved protease and serum stability. It caused concentration-dependent membrane permeabilization and depolarization, consistent with molecular dynamics simulations indicating aromatic-assisted anchoring and stable insertion. In murine infection models, W2PG achieved efficacy comparable to polymyxin B without observable organ toxicity. These results suggest that β-turn-guided design can balance stability, selectivity, and activity, providing a useful scaffold for peptide antibiotic development.

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Cell Host & Microbe · 2026 · IF 23.2

Gut DNA virome enterotype dictates inflammation heterogeneity through tuning the phage-bacteria-sphingosine-intestine axis in Crohn's disease

Weijie Wen,Runping Su,Yunyun Liu,Zhiyang Feng,Yancai Li,Jieli Li,Ziyu Huang,Fen Zhang,Shanshan Gao,Yingfei Ma,Qinghua Zhou,Emad M. El-Omar,Jeremy J. Barr,Tao Zuo

The human gut harbors a diverse virome, believed to play a crucial role in maintaining intestinal homeostasis. However, the magnitude of heterogeneity of the gut mucosal virome, and how it differentially regulates host inflammation phenotypes, such as those observed in Crohn’s disease (CD), remains unclear. Here, we identify two mucosal DNA virome enterotypes (E1 and E2) in humans, with E2 subjects exhibiting higher virome diversity and nuanced bacteriophage-bacteria correlations. Moreover, E2-enterotyped CD patients exhibited higher Wulfhauvirus abundance than healthy controls. The E2 virome is causally more proinflammatory in inducing intestinal inflammation in mice. Mechanistically, the novel E2-virome-enriched phage øBTZT001P (belonging to Wulfhauvirus ) lysogenically infects Bacteroides thetaiotaomicron , increasing sphingosine production. Downstream, sphingosine suppresses the commensal bacterium Blautia obeum in the gut, leading to worsened intestinal inflammation. Our findings reveal that configurational differences in the gut virome may dictate disease outcome through a phage-bacteria-metabolite-intestine axis, highlighting the importance of gut phage-bacteria crosstalk in health.

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NEW JOURNAL OF CHEMISTRY · 2026 · IF 2.6

Fe 3 O 4 magnetic core-shell nanoparticles -a new type of antibacterial material with both cell membrane targeting and synergistic photothermal-antibiotic effects

Yiting Geng,Yiwei Wang,Qingyu Meng,Ningbo Huang,Shan Huang,Xiaojun Chen

Conventional antimicrobial strategies relying on multiple antibiotics are becoming increasingly ineffective against drug-resistant strains, highlighting the urgent need for non-antibiotic-dependent therapeutic approaches. In this context, nanotechnology-based multifunctional platforms have emerged as a promising frontier in antimicrobial research due to their resistance-free mechanisms, high controllability, and precise targeting capability. This study presents a multifunctional nanoscale system, Fe₃O₄@polydopamine -Vancomycin @DC 2.4 cell membrane (FPVM), designed for the enrichment, recognition, and synergistic eradication of S. aureus. The system features an Fe 3 O 4 core coated with polydopamine, which enhances both photothermal performance and biocompatibility. Vancomycin is subsequently conjugated to the surface to enable specific recognition and bactericidal activity. Finally, the nanoparticles are encapsulated with stimulated dendritic cell (DC) membranes, further reinforcing the targeting ability toward S. aureus. Under 808 nm near-infrared irradiation (1.2 W cm -2 ), the FPVM platform (400 µg mL -1 ) reduced the survival rate of S. aureus to below 5% within 9 h and disrupted over 90% of pre-formed biofilms, demonstrating high photothermal conversion efficiency. In summary, the FPVM system integrates enhanced targeting and antibacterial functions, offering a versatile blueprint for constructing next-generation antimicrobial platforms.

CAS / MDL: 1404-90-6
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