title stringlengths 1 1.19k | keywords stringlengths 0 668 | concept stringlengths 0 909 | paragraph stringlengths 0 61.8k | PMID stringlengths 10 11 |
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Study procedure | A participant’s intravenous cannula was inserted into a vein in the right arm (dose escalation group) or a vein catheter (dose expansion group) for administration or top-up of the study drug. Only patients in the ciprofol group required an open vein in the left arm for blood collection for PK analysis. A simultaneous a... | PMC10147789 | ||
End points | SECONDARY | The primary end-point was the success rate of induction of general anesthesia produced by the initial bolus dose, i.e. the percentage of patients who achieved successful induction after the initial bolus dose, without requiring a top-up dose.The secondary end-points were: (1) the time to reach a MOAA/S ≤ 1, defined as ... | PMC10147789 | |
Measurements | DBP and mean arterial blood pressure, pain | The pain associated with a ciprofol or propofol injection was assessed approximately 15 s after initiation of the bolus injection. MOAA/S scores were recorded every 1 min and the eyelash reflex every 30 s.Hemodynamic parameters including HR, SBP, DBP and mean arterial blood pressure (MAP) were recorded at intervals of ... | PMC10147789 | |
Emergence time | Once surgery was completed, the MOAA/S score was assessed every 2 min until patients’ MOAA/S scores reached 5. | PMC10147789 | ||
Drugs | PMC10147789 | |||
Investigational drugs | Ciprofol emulsion (20 mL: 200 mg in part 1, and 20 mL: 50 mg in part 2 (Liaoning Haisco Pharmaceutical Group Co., Ltd., China) and Diprivan® (20 mL: 200 mg, AstraZeneca, UK).Midazolam (Jiangsu Nhwa Pharmaceutical Co., Ltd., China), sufentanil (Yichang Humanwell Pharmaceutical Co., Ltd., China) and rocuronium bromide (E... | PMC10147789 | ||
Statistical analysis | Wilson’s | IBM SPSS (ver. 25) was used for all statistical analyses. The demographic characteristics were analyzed using analysis of variance (ANOVA), chi-square, Fisher or Kruskal–Wallis tests. The primary outcome was also analyzed using Wilson’s and/or Fisher tests. Time to MOAA/S ≤ 1 and loss of the eyelash reflex were evaluat... | PMC10147789 | |
Results | PMC10147789 | |||
Demographic characteristics of patients in the dose escalation and dose expansion groups | From December 2016 to July 2018, a total of 109 patients for inclusion in both part 1 and part 2 were enrolled and the flow chart is shown in Fig. Flow chart of patient enrollment | PMC10147789 | ||
Efficacy | PMC10147789 | |||
Primary outcome | The success rates of anesthesia induction in patients who received one initial bolus dose of ciprofol-0.5 mg/kg, propofol-2.0 and 2.5 mg/kg were all 100%. However, 1 patient in the ciprofol-0.4 mg/kg group (part I) and one in the ciprofol-0.3 mg/kg group (part II) required one top-up dose and then achieved successful i... | PMC10147789 | ||
Secondary outcomes | All of the patients who received an initial bolus reached MOAA/S scores ≤ 1 at the end of the first min of administration except for 2 patients (1 in the 0.4 mg/kg ciprofol group and the other in the 2.0 mg/kg propofol group), who achieved MOAA/S scores ≤ 1 at the end of the second min of drug administration).As shown ... | PMC10147789 | ||
Discussion | pain | Propofol has been reported to have a narrow therapeutic index and the guidelines recommend usage only by experienced anesthesiologists, with close monitoring and individual dose adjustments [The main finding of the present study was that the success rates of induction with ciprofol-0.5 mg/kg as an i.v. bolus was compar... | PMC10147789 | |
Conclusion | The efficacy and safety of a single i.v. bolus dose of 0.5 mg/kg ciprofol for the induction of general anesthesia in patients undergoing selective surgery was comparable to propofol administered at a dose of 2.0 mg/kg. Lower doses of ciprofol, 0.3 mg/kg or 0.4 mg/kg, could also achieve the same efficacy but occasionall... | PMC10147789 | ||
Acknowledgements | We would like to thank other investigators Yuan Zeng, Tingting Jiang, ZhaoTing Meng, Rufeng Zeng, Huacheng Liu, Dingxin Kang, Li Yang, Yunxia Hu, Weixiang Min, Lu Jiang, Qiang Xu, Qingping Wu, Zhenghua Zhao, Yanling Jin, Fang Wang, Lili Wang, Saiying Wang, Huan Chang, and Kaiming Duan for their great assistance with th... | PMC10147789 | ||
Funding | This work was supported by the Sichuan Haisco Pharmaceutical Group Co., Ltd. The funder had no role in the design of the study, collection, analysis or interpretation of the data or in writing the manuscript. | PMC10147789 | ||
Conflicts of interest | The authors have no relevant financial or non-financial interests to disclose. | PMC10147789 | ||
References | PMC10147789 | |||
Background | NKTL, PTCL, Natural killer/T-cell lymphoma, peripheral T-cell lymphoma, NHL | PERIPHERAL T-CELL LYMPHOMA, NHL | Natural killer/T-cell lymphoma (NKTL) is a rare type of aggressive and heterogeneous non-Hodgkin's lymphoma (NHL) with a poor prognosis and limited therapeutic options. Therefore, there is an urgent need to exploit potential novel therapeutic targets for the treatment of NKTL. Histone deacetylase (HDAC) inhibitor chida... | PMC9900953 |
Methods | NKTL, tumors | TUMORS | We performed a phase II clinical trial to evaluate the efficacy of chidamide in 28 relapsed/refractory NKTL patients. Integrative transcriptomic, chromatin profiling analysis and functional studies were performed to identify potential predictive biomarkers and unravel the mechanisms of resistance to chidamide. Immunohi... | PMC9900953 |
Results | NKTL, hyperactivity | We demonstrated that chidamide is effective in treating relapsed/refractory NKTL patients, achieving an overall response and complete response rate of 39 and 18%, respectively. In vitro studies showed that hyperactivity of JAK-STAT signaling in NKTL cell lines was associated with the resistance to chidamide. Mechanisti... | PMC9900953 | |
Supplementary Information | The online version contains supplementary material available at 10.1186/s13148-023-01436-6. | PMC9900953 | ||
Keywords | PMC9900953 | |||
Introduction | Natural killer/T-cell lymphoma, NKTL, Barr virus-associated T-cell lymphoma | EPSTEIN | Natural killer/T-cell lymphoma (NKTL) is an aggressive Epstein–Barr virus-associated T-cell lymphoma (TCL) that accounts for 10% of all TCLs [Histone acetylation is an important mode of epigenetic regulation controlled by the antagonistic actions of two classes of enzymes: histone acetyltransferases (HATs) and histone ... | PMC9900953 |
Methods | PMC9900953 | |||
Patients and cell lines | NKTL, tumor, Cancer | MYCOPLASMA, MYCOPLASMA, TUMOR, CANCER | A phase II clinical trial to evaluate chidamide monotherapy in relapsed/refractory NKTL was conducted at Sun Yat-sen University Cancer Center (SYSUCC). The study was approved by the institutional review board of SYSUCC in accordance with the Declaration of Helsinki, and applicable regulations according to Good Clinical... | PMC9900953 |
Drugs | ALDRICH | Chidamide was provided by Shenzhen Chipscreen Biosciences Ltd. SAHA was obtained from Sigma–Aldrich. Trichostatin A (TSA), belinostat and tofacitinib were purchased from Selleckchem. Romidepsin was obtained from MedChemExpress. Ruxolitinib and Stattic were purchased from Axon Medchem and Millipore, respectively. | PMC9900953 | |
Cell viability assays | Tecan | PROLIFERATION | A total of 2000 cells were seeded in 96-well plates in triplicate and treated with the indicated drugs at various concentrations or not treated for 96 h. Cell viability was measured by the CellTiter-Glo Luminescent Cell Viability Assay (Promega) according to the manufacturer’s instructions, and luminescence was read us... | PMC9900953 |
Calculation of the combination index (CI) | CI values were determined by the inhibition rate of the cells treated with drugs and computed using CalcuSyn [ | PMC9900953 | ||
Cell cycle assays | 2 × 10 | PMC9900953 | ||
Cell apoptosis assay | 2 × 10 | PMC9900953 | ||
H&E staining and immunohistochemistry (IHC) | NKTL | EPSTEIN | H&E staining, IHC for TNFRSF8 (CD30) and Epstein–Barr encoding region in situ hybridization (EBER ISH) were performed with formalin-fixed, paraffin-embedded (FFPE) tissues from NKTL patients using standard procedures [ | PMC9900953 |
ChIP-qPCR, ChIP-seq and ChIP-seq data analyses | The primer sequences used for ChIP-qPCR are listed in Additional File | PMC9900953 | ||
Real-time RT–qPCR, RNA-seq and RNA-seq data analyses | The primer sequences used for RT–qPCR are listed in Additional File | PMC9900953 | ||
In vivo studies | In vivo studies were conducted in compliance with animal protocols approved by the SingHealth Institutional Animal Care and Use Committee. Five- to eight-week-old female NOD/SCID/IL2rγnull (NSG) mice were kept under standard laboratory conditions according to the National Advisory Committee for Laboratory Animal Resear... | PMC9900953 | ||
Statistical analysis | SD | Graphs include results that are expressed as the mean ± SD of three independent experiments. Statistical differences between the two groups were evaluated by a two-tailed Student’s | PMC9900953 | |
Results | PMC9900953 | |||
Clinical efficacy of chidamide, a novel HDAC inhibitor, in relapsed/refractory NKTL patients | NKTL | DISEASE PROGRESSION | To evaluate the efficacy of chidamide, a single-arm, phase II clinical trial was performed in 28 NKTL patients who relapsed after or were refractory to chemoradiotherapy and/or autologous stem cell transplantation (ASCT). The patients were treated with chidamide until disease progression or intolerance. The demographic... | PMC9900953 |
Characterization of NKTL cell line sensitivity to chidamide in vitro | NKTL, death | PROLIFERATION | To assess the in vitro efficacy of chidamide in NKTL, we evaluated the IC50 of the drug in 11 NKTL cell lines (Fig. Chidamide inhibits cell proliferation and selectively induces the death of NKTL cells. | PMC9900953 |
Enhancer landscapes in chidamide-resistant and chidamide-sensitive cells | NKTL | To investigate the underlying mechanism of resistance to chidamide in NKTL cells, we performed chromatin immunoprecipitation sequencing (ChIP-seq) for H3K27ac and H3K4me3 in two resistant cell lines (HANK1 and SNK6) and two sensitive cell lines (KHYG1 and MEC04). Epigenetic changes in H3K27ac and H3K4me3, which are ass... | PMC9900953 | |
Aberrant activation of the JAK-STAT pathway in NKTL | NKTL | As the JAK-STAT pathway was found to be implicated in resistance to chidamide, we examined the activity of its effector molecules, STAT3 and STAT5 in both sensitive and resistant NKTL cell lines. High levels of phospho-STAT3 and STAT5 were detected in resistant cell lines compared to sensitive cell lines (Fig. The JAK-... | PMC9900953 | |
Pharmacologically targeting the JAK-STAT pathway overcomes resistance to chidamide in NKTL | NKTL | We hypothesized that targeting the JAK-STAT pathway could reverse chidamide resistance in NKTL cell lines. To test this hypothesis, we treated the chidamide-resistant NKTL cell lines (HANK1 and SNK6) with tofacitinib (JAK inhibitor), chidamide or a combination of both drugs for 96 h and determined the combination index... | PMC9900953 | |
The JAK inhibitors tofacitinib/ruxolitinib induce chromatin remodeling at JAK-STAT genes | NKTL | To understand how JAK inhibitors reverse chidamide resistance in NKTL cells, we performed RNA-seq of HANK1 cells treated with DMSO, tofacitinib or ruxolitinib. Compared to the control treatment, tofacitinib and ruxolitinib treatment remarkably upregulated 131 common genes and downregulated 141 common genes in HANK1 cel... | PMC9900953 | |
Clinical efficacy of JAK-STAT inhibition and chidamide in chidamide-resistant NKTL | NKTL, death | EPSTEIN, VIRUS, DISEASE | We next assessed whether JAK-STAT inhibition could be a potential therapeutic strategy to overcome resistance to chidamide in the clinic. A 48-year-old Chinese male patient who was initially diagnosed with stage IIA extranodal NKTL of the nasal type was recruited. He was refractory to first-line asparaginase-based chem... | PMC9900953 |
Discussion | NKTL, tumor, H3Y41, PTCL | DISORDER, REGRESSION, DISEASE, TUMOR | In the current management of NKTL, a substantial proportion of patients still experience treatment failures, and salvage options are severely limited. Increasing evidence suggests that PTCL is characteristically an epigenetic disorder, with several HDAC inhibitors receiving regulatory approvals for the treatment of rel... | PMC9900953 |
Conclusions | NKTL | In summary, our study shows favorable clinical outcomes of chidamide in treating relapsed/refractory NKTL patients. JAK-STAT inhibitors may further expand the clinical utility of HDAC inhibitors, including chidamide, romidepsin and belinostat, by remodeling the resistant enhancer landscape toward a sensitive state. The... | PMC9900953 | |
Acknowledgements | We thank Shenzhen Chipscreen Biosciences Ltd. for providing us with chidamide for our work. We thank Dr. Yoshitoyo Kagami, Dr. C. Clayberger, Dr. Norio Shimizu, Dr. Paul Coppo and Dr. Philippe Gaulard for kindly providing the cell lines used in this study. | PMC9900953 | ||
Author contributions | PD | PATHOLOGY | JC, HH, CKO and JT conceived, designed and supervised the study; JC, YG, ZL, YW and KXYC performed the experiments; JC, ZZ, YG, XY, PG, ZL, JH, PD, JYC, JL, BKHC, HH, CKO and JT analyzed and interpreted the data; YG, XL and HH provided samples; XY, JH, DC, JWP, JK, DH, HH, YS, LL, SL, XW, HY, NFG, JB, TK, STL and BTT p... | PMC9900953 |
Funding | Cancer | CANCER | This work was supported by the National Natural Science Foundation of China (81970176, 81972596 and 81772963), Guangdong Innovative and Entrepreneurial Research Team Program (2016ZT06S638 and 2016ZT06S252), Sci-Tech Project Foundation of Guangzhou City (201707020039), Medical Scientific Research Foundation of Guangdong... | PMC9900953 |
Availability of data and materials | The datasets supporting the conclusions of this article are available at GEO under accession number GSE152185. | PMC9900953 | ||
Declarations | PMC9900953 | |||
Ethics approval and consent to participate | tumor | TUMOR | The study was approved by the institutional review board of SYSUCC in accordance with the Declaration of Helsinki, and applicable regulations according to Good Clinical Practice guidelines. Written informed consent was obtained from all patients before enrollment in the trial. This trial was registered at ClinicalTrial... | PMC9900953 |
Consent for publication | All authors have agreed to publish this manuscript. | PMC9900953 | ||
Competing interests | The authors declare that they have no competing interests. | PMC9900953 | ||
References | PMC9900953 | |||
Background | HGP1705, acid-related disorders | EROSIVE ESOPHAGITIS | Proton-pump inhibitors (PPIs) are the most effective drugs for treating acid-related disorders. However, once-daily dosing with conventional PPIs fail to fully control acid secretion over 24 h. This study aimed to compare the efficacy and safety of HIP1601 (dual delayed-release esomeprazole) and HGP1705 (delayed-releas... | PMC10729464 |
Methods | treatment-emergent adverse, HGP1705, GERD-related | We enrolled 213 patients with EE randomized in a 1:1 ratio to receive 40 mg HIP1601 (n = 107) or HGP1705 (n = 106) once daily for 4 or 8 weeks. The primary endpoint was the EE healing rate, confirmed by endoscopy up to week 8. GERD-related symptoms and treatment-emergent adverse events were compared between both groups... | PMC10729464 | |
Results | HGP1705 | By week 8, the estimated healing rates of EE were 97.8% and 96.8% in the HIP1601 and HGP1705 groups, respectively, with a 95% confidence interval of -4.7 to 7.2. After 4 or 8 weeks of treatment, the EE healing rate at week 4, complete resolution rate of symptoms, time to sustained resolution of symptoms, and number of ... | PMC10729464 | |
Conclusions | HGP1705 | GERD | The efficacy and safety of HIP1601 40 mg were comparable to those of HGP1705 40 mg for the treatment of EE and symptomatic improvement of GERD. | PMC10729464 |
Trial registration | NCT04080726 ( | PMC10729464 | ||
Supplementary Information | The online version contains supplementary material available at 10.1186/s12876-023-03087-6. | PMC10729464 | ||
Keywords | PMC10729464 | |||
Background | chronic disorder, heartburn, GERD, acid regurgitation, Barrett’s esophagus [HIP1601, esophagitis, Barrett’s esophagus, reflux of gastric | CHRONIC DISORDER, ESOPHAGEAL STRICTURE, GERD, ESOPHAGITIS, GASTROESOPHAGEAL REFLUX DISEASE (GERD), COMPLICATIONS | Gastroesophageal reflux disease (GERD) is a chronic disorder caused by the reflux of gastric contents, resulting in symptoms such as heartburn and acid regurgitation as well as potential complications such as esophagitis and Barrett’s esophagus [Proton pump inhibitors (PPIs) are the most commonly prescribed class of me... | PMC10729464 |
Materials and methods | PMC10729464 | |||
Study design | treatment-emergent adverse, HGP1705, GERD-related | EROSIVE ESOPHAGITIS, HEART | This study was designed as a multicenter, double-blind, randomized controlled, non-inferiority trial involving patients with erosive esophagitis (EE). Patients with EE were randomly assigned to receive either HIP1601 40 mg or HGP1705 40 mg for 4 or 8 weeks. Complete EE healing rates, GERD-related symptoms, and treatmen... | PMC10729464 |
Study subject | primary esophageal motility disorders, heartburn, malignancy, acid regurgitation, active gastric or, Zollinger-Ellison syndrome, Barrett’s esophagus, duodenal ulcer | ESOPHAGEAL DYSPLASIA, GASTROINTESTINAL BLEEDING, ZOLLINGER-ELLISON SYNDROME, INFLAMMATORY BOWEL DISEASE | Male and female patients aged 19–75 years were eligible for inclusion if they had endoscopically confirmed EE based on the Los Angeles (LA) Classification (grades A–D). Additionally, patients had to experience symptoms of acid regurgitation and/or heartburn 7 days prior to the screening visit.The exclusion criteria for... | PMC10729464 |
Study protocol | Figure
Randomization protocol and patient disposition | PMC10729464 | ||
Efficacy and safety assessment | GERD, death, TEAEs, disability | ADVERSE EVENTS, ADVERSE EVENT, GERD, REMISSION, ADVERSE EVENT | The primary endpoint of the study was the complete healing rate of EE confirmed endoscopically up to week 8 in the per-protocol set (PPS) population. The complete healing of EE was defined as the LA Classification criterion “Not Present” in endoscopy after administration of the clinical trial drug [Patients were instru... | PMC10729464 |
Statistical analyses | HGP1705 | For estimating the necessary number of subjects, the complete healing rate of EE by week 8 was assumed to be 93.7% in the HGP1705 40 mg group [Safety analysis was conducted among those who took at least one dose of the clinical trial drugs after random assignment, for whom data on safety assessments could be obtained. ... | PMC10729464 | |
Results | PMC10729464 | |||
Study population and baseline characteristics | GASTROESOPHAGEAL REFLUX DISEASE | In total, 213 patients were enrolled in this clinical trial (Fig. Table
Baseline patient demographics and characteristics according to treatment groupGERD, Gastroesophageal reflux disease; LA, Los Angeles; SD, standard deviation | PMC10729464 | |
Primary endpoint | HGP1705 | EROSIVE ESOPHAGITIS | Based on the PPS analysis by week 8, the complete healing rate of EE in the HIP1601 group was 97.8% (91/93), which was higher than the rate of 96.8% (91/94) in the HGP1705 group (Table
Healing rate of erosive esophagitis by weeks 8 and 4EE, erosive esophagitis; CI, confidence interval; FAS, full analysis set; PPS, per... | PMC10729464 |
Secondary endpoints | PMC10729464 | |||
Healing rate of erosive esophagitis at week 4 | HGP1705 | In PPS analysis at week 4, the complete healing rate of EE in the HIP1601 and HGP1705 groups were 91.4% (85/93) and 92.6% (87/94), respectively, and the 95% CI of the difference between the two groups ranged from − 8.9 to 6.6 (Table | PMC10729464 | |
Complete resolution rate of GERD symptoms at week 4 or 8 | dysphagia, HGP1705, heartburn, GERD, acid regurgitation, pain | DYSPHAGIA, GERD | After 4 weeks of treatment, the complete resolution rate of overall GERD symptoms, including heartburn, acid regurgitation, dysphagia, and epigastric pain, was 49.5% (46/93) in the HIP1601 group and 48.9% (46/94) in the HGP1705 group (Table
Complete resolution rate of symptoms after treatment (per protocol set)46(49.5... | PMC10729464 |
Proportion of heartburn- and acid regurgitation-free days and nights by week 1, 2, 4, 8 (per protocol set) | HGP1705 | The proportions of heartburn- and acid regurgitation-free days by week 4 were 68.1% and 68.7% in HIP1601 group, and 71.9% and 69.3% in HGP1705 group, respectively (Fig.
The proportion of symptoms-free days and nights after 1, 2, 4 weeks of treatment (per protocol set). A, the proportion of heartburn-free days after 1,... | PMC10729464 | |
Time to sustained resolution of heartburn and acid regurgitation (per protocol set) | HGP1705, heartburn | The median time to sustained resolution of heartburn was 7 days (95% CI: 3.0–16.0) in the HIP1601 group and 8 days (95% CI: 5.0–11.0) in the HGP1705 group (Supplementary Table The proportion of patients who achieved sustained resolution of nocturnal heartburn and nocturnal acid regurgitation was 87.2% (34/39) and 81.8%... | PMC10729464 | |
Number of rescue medication use | HGP1705 | The mean number of rescue medications administered in the HIP1601 (7.8 per subject) was lower than that (9.3 per subject) in the HGP1705 group. However, there was no significant difference between the two groups ( | PMC10729464 | |
Tolerability and safety | HGP1705, TEAEs | ADVERSE EVENTS, EVENTS, ADVERSE EVENT | The incidence of TEAEs was 14.3% (15/105; 22 events) in the HIP1601 group and 14.2% (15/106; 20 events) in the HGP1705 group (Table
Summary of treatment-emergent adverse events (safety analysis set)TEAE: treatment-emergent adverse events*TEAEs: Adverse events with start date on or after administration of the study dru... | PMC10729464 |
Discussion | GERD, fracture, TEAEs, erosions, hypomagnesemia, reflux disease, NERD, community-acquired pneumonia, Barrett’s esophagus, esophageal and extraesophageal symptoms, gastric acid | ADVERSE EVENTS, GERD, HYPOMAGNESEMIA, CLOSTRIDIUM DIFFICILE INFECTION, COMMUNITY-ACQUIRED PNEUMONIA, COMPLICATIONS | The goal of GERD treatment is to alleviate symptoms and prevent complications. Although currently approved delayed-release PPIs have shown benefits in the treatment of GERD, unmet needs remain [Although a new class of drugs, such as potassium-competitive acid blockers (P-CABs), has recently been developed, PPIs remain ... | PMC10729464 |
Conclusions | GERD, HGP1705 | GERD | In conclusion, the findings of this study support the efficacy and safety of HIP1601 40 mg as a treatment option for EE healing and alleviating GERD symptoms. The results indicate that HIP1601 is not inferior to HGP1705 40 mg in terms of both efficacy and safety, as demonstrated by comparable healing rates and tolerabi... | PMC10729464 |
CONSORT guidelines | The study adheres to the CONSORT guidelines and a completed CONSORT has been submitted separately. | PMC10729464 | ||
Electronic supplementary material | Below is the link to the electronic supplementary material.
Supplementary Material 1 | PMC10729464 | ||
Acknowledgements | Not applicable. | PMC10729464 | ||
Author contributions | Hwoon-Yong Jung: Study concept and design, study supervision, acquisition of data, revision of the manuscript, statistical analysis, interpretation of data, verified the underlying data. Hyun Lim: Acquisition of data, drafting of the manuscript, revision of the manuscript, interpretation of data,. Jae Myung Park, Jong ... | PMC10729464 | ||
Funding | This work was supported by Hanmi Pharmaceuticals Co., Ltd., Seoul, Republic of Korea (HM-ESOM-301). | PMC10729464 | ||
Data availability | Relevant data have been presented in the main manuscript. The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request. | PMC10729464 | ||
Declarations | PMC10729464 | |||
Ethics approval and consent to participate | The study protocol was approved by the ethics committees of all participating hospitals. | PMC10729464 | ||
Consent for publication | Informed consent was obtained from all individual participants included in the study. | PMC10729464 | ||
Competing interests | The authors declare no competing interests. | PMC10729464 | ||
References | PMC10729464 | |||
Background | fibrosis, IUA | INTRAUTERINE ADHESIONS, FIBROSIS | Intrauterine adhesion (IUA) is a frequent acquired endometrial condition, for which there is no effective preventive or treatment. Previous studies have found that vaginal microbiota dysregulation is closely related to endometrial fibrosis and IUA. Therefore, we wondered whether restoration of vaginal microbiota by vag... | PMC10032012 |
Results | IUA | First, we created a mechanically injured mouse model of IUA and restored the mice’s vaginal microbiota by the addition of | PMC10032012 | |
Conclusions | This study confirmed that | PMC10032012 | ||
Clinical trial registration | : | PMC10032012 | ||
Supplementary Information | The online version contains supplementary material available at 10.1186/s12866-023-02823-y. | PMC10032012 | ||
Keywords | PMC10032012 | |||
Results | PMC10032012 | |||
Discussion | TGF-β1, inflammation, fibrosis, intrauterine inflammation, infection, IUA, endometrial basal layer damage | ENDOMETRITIS, INTRAUTERINE ADHESION, INFLAMMATION, FIBROSIS, INFECTION | Finally, 10 vaginal secretion samples were selected in the group C, I, E and L, a total of 40 samples were used for high-throughput sequencing. In α-diversity, there are significant differences in Shannon (P < 0.01) and Simpson (P < 0.005) (Fig.
The effect of We allow visitors to reproduce images with permission and/... | PMC10032012 |
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