IntroductionPropofol may induce emotional impairment like euphoria and elation. Previous studies have demonstrated that emotional impairment can injure social cognition like emotion recognition and decision-making abilities. Therefore, this study is designed to investigate the effects of propofol anesthesia on facial emotion recognition (FER) and delay discounting behavior.MethodPatients underwent diagnostic gastrointestinal endoscopy (GI) with propofol anesthesia in this prospective cohort observational study. Prior to and following the procedure (approximately 30 min afterwards), patients were asked to select the word that best describes the presented facial photographs displaying happiness, anger, and neutral expressions. Additionally, Monetary Choice Questionnaire-9 was used to assess delay discounting.ResultsWithin a cohort of 87 patients, 11 patients (12.6%) met the criterion of FER deficit post-GI. The FER of anger exhibited significant differences between pre- and post-GI, considering both the correct (52.6%) and incorrect (24.3%) recognition. There was a positive identification bias for FER after propofol anesthesia: mistaking anger (p = 0.02) or neutral (p = 0.01) expression for happiness. Procedures in the morning and the absence of insomnia were associated with the decreased FER score of anger post-GI. The results did not indicate any impairment of propofol anesthesia on FER of happiness or delay discounting behavior.ConclusionThe study demonstrates that propofol anesthesia during GI endoscopy selectively impairs the recognition of anger facial expressions while leaving the recognition of happiness and delay discounting unaffected at a short-term postoperative observation. Additionally, the recognition of anger and neutral facial expressions exhibited a tendency towards a positive bias.Clinical trial registrationhttps://www.chictr.org.cn/showproj.html?proj=199458, identifier ChiCTR2300073132.

Conventional endoscopy is widely used in the diagnosis of early gastric cancers (EGCs), but the graphical features were loosely defined and dependent on endoscopists’ experience. We aim to establish a more accurate predictive model for infiltration depth of early gastric cancer including a standardized colorimetric system, which demonstrates promising clinical implication. A retrospective study of 718 EGC cases was performed. Clinical and pathological characteristics were included, and Commission Internationale de l’Eclariage (CIE) standard colorimetric system was used to evaluate the chromaticity of lesions. The predicting models were established in the derivation set using multivariate backward stepwise logistic regression, decision tree model, and random forest model. Logistic regression shows location, macroscopic type, length, marked margin elevation, WLI color difference and histological type are factors significantly independently associated with infiltration depth. In the decision tree model, margin elevation, lesion located in the lower 1/3 part, WLI a*color value, b*color value, and abnormal thickness in enhanced CT were selected, which achieved an AUROC of 0.810. A random forest model was established presenting the importance of each feature with an accuracy of 0.80, and an AUROC of 0.844. Quantified color metrics can improve the diagnostic precision in the invasion depth of EGC. We have developed a nomogram model using logistic regression and machine learning algorithms were also explored, which turned out to be helpful in decision-making progress.

Background: Helicobacter pylori infection is one of the main causes of gastric cancer. thioredoxin-1 (Trx1) and arginase (RocF) expressed by H. pylori were found to be closely related to its pathogenicity. However, whether Trx1 and RocF can be used in clinical screening of highly pathogenic H. pylori and the pathogenesis of trx1 high expressing H. pylori remain still unknown. Materials and Methods: We investigated the expression level of H. pylori trx1 and H. pylori rocF in human gastric antrum tissues using reverse transcription and quantitative real-time PCR (RT-qPCR) and clarified the clinical application value of trx1 and rocF for screening highly pathogenic H. pylori. The pathogenic mechanism of Trx1 were further explored by RNA-seq of GES-1 cells co-cultured with trx1 high or low expressing H. pylori. Differentially expressed genes and signaling pathways were validated by RT-qPCR, Enzyme-linked immunosorbent assay (ELISA), western blot, immunohistochemistry and immunofluorescence. We also assessed the adherence of trx1 high and low expressing H. pylori to GES-1 cells. Results: We found that H. pylori trx1 and H. pylori rocF were more significantly expressed in the gastric cancer and peptic ulcer group than that in the gastritis group and the parallel diagnosis of H. pylori trx1 and H. pylori rocF had high sensitivity. The trx1 high expressing H. pylori had stronger adhesion ability to GES-1 cells and upregulated the interleukin (IL) 23A/nuclear factor kappa appaB (NF-kappa B)/IL17A, IL6, IL8 pathway. Conclusions: H. pylori trx1 and H. pylori rocF can be used in clinical screening of highly pathogenic H. pylori and predicting the outcome of H. pylori infection. The trx1 high expressing H. pylori has stronger adhesion capacity and promotes the development of gastric diseases by upregulating the activation of NF-kappa B signaling pathway.

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CagA, a virulence factor of Helicobacter pylori (H. pylori), is known to drive inflammation in gastric epithelial cells and is typically degraded through autophagy. However, the molecular mechanism by which CagA evades autophagy-mediated degradation remains elusive. This study found that H. pylori inhibits autophagic flux by upregulating the expression of AU-rich element RNA-binding factor 1 (AUF1). We confirmed that AUF1 does not affect autophagy initiation but instead hampers lysosomal clearance, as evidenced by treatments with 3-MA, CQ and BafA1. Upregulated AUF1 stabilizes CagA protein levels by inhibiting the autolysosomal degradation of intracellular CagA in H. pylori-infected gastric epithelial cells. Knocking down AUF1 promotes CagA degradation, an effect that can be reversed by the lysosome inhibitor BafA1 and CQ. Transcriptome analysis of AUF1-knockdown gastric epithelial cells infected with H. pylori indicated that AUF1 regulates the expression of lysosomal-associated hydrolase genes, specifically CTSD, to inhibit autolysosomal degradation. Moreover, we observed that knockdown of AUF1 enhanced the stability of CTSD mRNA and identified AUF1 binding to the 3’UTR region of CTSD mRNA. AUF1-mediated downregulation of CTSD expression contributes to CagA stability, and AUF1 overexpression leads to an increase in CagA levels in exosomes, thus promoting extracellular inflammation. In clinical gastric mucosa, the expression of AUF1 and its cytoplasmic translocation are associated with H. pylori-associated gastritis, with CagA being necessary for the translocation of AUF1 into the cytoplasm. Our findings suggest that AUF1 is a novel host-positive regulator of CagA, and dysregulation of AUF1 expression increases the risk of H. pylori-associated gastritis.

A dual-mode assay was developed for screening and detecting live Escherichia coli (E. coli) and Hafnia paralvei (H. paralvei) (as two typical pathogens in aquatic environments) based on magnetic poly(phages) encoded probes (MPEP). The probes were prepared by grafting a large number of phages targeting different target bacteria on a long-chain DNA structure, respectively. They could specifically capture and enrich E. coli and H. paralvei by magnetic separation. Then, different DNA signal tags with different lengths conjugate with the corresponding MPEP-bacteria complex and form two kinds of sandwich structures, respectively. After that, the captured E. coli and H. paralvei were lysed to release both adenosine triphosphate (ATP) and DNA signal tags. The measurement includes two steps. Firstly, a portable ATP bioluminescence meter was employed to rapidly screen the positive samples that contain either of the two target bacteria. Secondly, only positive samples were injected into the microfluidic chip which could detect various DNA signal tags for accurate quantification of the target bacteria. The assay demonstrated high sensitivity (3 CFU/mL for E. coli and 5 CFU/mL for H. paralvei), high specificity (strain identification), signal amplification (20-fold), and short time (≤ 35 min). It can be applied to detect other pathogens solely by changing the relative phage in MPEP. Furthermore, the proposed dual-mode assay provides a wide prospect for rapid screening and accurate determination of live foodborne pathogens. Clinical Trial Number: nbdxms-20240322.

RNA modification C 2 -methyladenosine (m 2 A) exists in both rRNA and tRNA of Escherichia coli ( E. coli ), installed by the methyltransferase RlmN using a radical- S -adenosylmethionine (SAM) mechanism. However, the precise function of m 2 A in tRNA and its ubiquity in plants have remained unclear. Here we discover the presence of m 2 A in chloroplast rRNA and tRNA, as well as cytosolic tRNA, in multiple plant species. We identify six m 2 A-modified chloroplast tRNAs and two m 2 A-modified cytosolic tRNAs across different plants. Furthermore, we characterize three Arabidopsis m 2 A methyltransferases—RLMNL1, RLMNL2, and RLMNL3—which methylate chloroplast rRNA, chloroplast tRNA, and cytosolic tRNA, respectively. Our findings demonstrate that m 2 A37 promotes a relaxed conformation of tRNA, enhancing translation efficiency in chloroplast and cytosol by facilitating decoding of tandem m 2 A-tRNA-dependent codons. This study provides insights into the molecular function and biological significance of m 2 A, uncovering a layer of translation regulation in plants.

BACKGROUND:Hyperplastic polyps, which represent 30%-93% of all gastric epithelial polyps, are the second most common type of gastric polyps after fundic gland polyps. They were previously considered to have no risk of neoplastic transformation. Recently, an increasing number of cases of gastric hyperplastic polyps (GHPs) combined with neoplastic changes have been reported; however, the specific mechanism underlying their transformation has not been thoroughly explored. AIM:To investigate the clinical, endoscopic, and pathological characteristics of the neoplastic transformation of GHPs and explore the risk factors. METHODS:A retrospective analysis was performed on 4010 cases of GHPs diagnosed by gastroscopy and pathological examination at the hospital from 2005 to 2021. In total, 3874, 119, and 17 cases were in the group without intraepithelial neoplasia (IN), with low-grade IN, and with high-grade IN, respectively. The data analysis examined the association of endoscopic and pathological features with risk factors for neoplastic transformation. Factors with significant differences were entered into univariate logistic regression, followed by multivariate logistic regression analysis. RESULTS:Univariate analysis revealed diameter, multiple polyp presence, redness, rough surface, lobulation, erosion, Yamada classification, location, and gastric mucosa were risk factors for neoplastic transformation. Multivariate analysis showed that age > 65 years [odds ratio (OR) = 1.789; 95% confidence interval (CI): 1.227-2.609; P = 0.003], male sex (OR = 1.680; 95%CI: 1.158-2.438; P = 0.006), multiple polyps (OR = 1.851; 95%CI: 1.230-2.784; P = 0.003), pedunculated or semi-pedunculated shape (OR = 2.722; 95%CI: 1.689-4.388; P < 0.001), and polyp diameter were significantly associated with GHPs that demonstrated neoplastic transformation. Compared with chronic superficial gastritis, autoimmune gastritis, atrophic gastritis, and gastritis with IN were independent risk factors for neoplastic transformation [(OR = 2.672; 95%CI: 1.559-4.579; P < 0.001), (OR = 1.876; 95%CI: 1.134-3.103; P = 0.014), and (OR = 5.299; 95%CI: 3.173-8.849; P < 0.001), respectively]. CONCLUSION:Male sex, age > 65 years, multiple polyps, pedunculated or semi-pedunculated shape, polyp size > 1 cm, and specific background gastric mucosa are key indicators for predicting neoplastic transformation of GHPs.

目的 比较内镜黏膜下剥离(endoscopic submucosal dissection,ESD)与外科手术治疗早期胃癌的安全性和预后.方法 收集2010 年1 月～2018 年 10 月我院因早期胃癌行ESD 213 例以及外科手术 209 例的临床资料,进行倾向性评分匹配,2 组各95 例,比较ESD及外科手术的安全性及预后.结果 ①原始队列中,ESD组中位随访时间21(10,46)月,外科手术组54(30,85)月(Z =-8.985,P =0.000),ESD组与外科手术组总生存率无显著差异(97.6％vs.96.5％,log-rank χ2 = 0.772,P =0.380),但无复发生存率显著低于外科手术组(94.8％vs.98.4％,log-rank χ2 =4.667,P =0.031).经倾向性评分匹配后,ESD组与外科手术组的总生存率和无复发生存率均无显著差异(100％vs.97.4％,log-rank χ2 =0.671,P =0.413;98.6％vs.97.7％,log-rank χ2 =0.023,P =0.879).②原始队列中,ESD组手术时间显著小于外科手术组[58(55,90)min vs.270(210,315)min,Z =-15.974,P =0.000],住院日较外科手术组显著缩短[11(9,13)d vs.18(14,22)d,Z =-13.428,P = 0.000],术后转入ICU的比例显著低于外科手术组[1.4％(3/213)vs.18.2％(38/209),χ2 =33.835,P =0.000],倾向性评分匹配后这些指标2 组差异仍有统计学意义(均P =0.000).结论 ESD与外科手术治疗早期胃癌的远期疗效相当,且ESD手术时间短,术后进ICU比例低,住院日短.

The survival rate of early gastric cancer and esophageal cancer is more than 90%. Confocal endoscopy can detect cell morphology and mucosal glandular structure (depth about 500 μm), presenting a cross-sectional microscopic image unfamiliar to both endoscopists and pathologists. Therefore, using computer-aided diagnosis technology to complete real-time artificial intelligence diagnosis of early esophageal and gastric cancer is of great significance for early detection and early treatment of cancer patients. ResNet convolution neural network based image classification model, the introduction of attention mechanism based on CBAM module to improve the performance of the model, to achieve intelligent diagnosis of confocal endoscopy images.

Indolent T-cell lymphoproliferative disorder of the gastrointestinal tract (iTLPD-GI) is a rare neoplasm usually having an indolent clinical course and easily misdiagnosed as inflammatory bowel disease or other T-cell lymphomas. A subset of the disorders that progressed to overt peripheral T-cell lymphoma have been reported, and the etiology and pathogenesis are poorly understood. The current study retrospectively examined the pathological, molecular, and clinical features of 6 cases of iTLPD-GI. Hematoxylin and eosin staining, immunohistochemistry, in situ hybridization, T-cell receptor gene rearrangement, and next-generation sequencing (NGS) were performed with the diseased tissues. All the 6 patients were immunocompetent Chinese men, who presented with recurrent abdominal pain and diarrhea for 4 to 13 years. Histologically, the intestinal tissue was expanded by lymphoid infiltration, composed of small-to-medium-sized lymphocytes with gland intact. The neoplastic cells were CD4 − /CD8 + with expression of TIA1 and variable granzyme B in five cases, and the other one was CD4 + /CD8 − . Two of the 5 patients progressed to more aggressive T-cell lymphoma and died of disease with complications. NGS identified TET2 and DDX3X mutations in patient 1, and BIRC6 and REV3L mutations in patient 2. Literature review indicated that iTLPD-GI with CD4 − /CD8 + immunophenotype was more commonly reported in Chinese cases. Our limited data indicated CD4-/CD8 + iTLPD-GI have similar potential to progress to more aggressive T-cell lymphoma as that of CD4 + /CD8 − , and gradually increased expression of granzyme B and Ki-67 may be early signs of the disease progression. Gain of novel gene mutations may be indicators of the pathogenesis.

According to the Correa model, the intestinal-type gastric cancer (GC) is preceded by premalignant lesions, including chronic gastritis, intestinal metaplasia and dysplasia. However, the dynamic change of innate and adaptive immune response during this process has not been studied comprehensively. In this study, we performed a comprehensive and trajectory analysis of circulating innate lymphoid cells (ILCs) and adaptive Th lymphocytes subtypes in patients spanning a cascade of gastric lesions. Increased circulating ILC2s frequency was found in the gastritis, premalignant stage and GC group, whereas further decreased ILC2s were detected in the GC group compared with the premalignant group. Moreover, ILC3s level was higher in both gastritis, premalignant lesion and GC stage, compared with healthy controls. Furthermore, up-regulated T follicular helper (Tfh) cell proportions were detected in the gastritis and premalignant process. In conclusion, by analyzing the circulating ILCs and Th cells frequency and the key cytokine production or immunoglobulin level, we demonstrated the potential involvement of ILC3 and Tfh in the gastric diseases. These findings will help to understand the immunologic mechanisms in both GC and the premalignant process and contribute to serve potential therapeutic targets to prevent the GC development.

胃腺癌和胃淋巴瘤是2 种最常见的胃恶性肿瘤,发生和发展均与幽门螺杆菌( Helicobacter pylori, H.pylori)感染有关,但胃淋巴瘤合并胃腺癌非常罕见[1].本文报道1 例胃原发性弥漫大B 细胞淋巴瘤( primary gastric-diffuselarge B-cell lymphoma , PG-DLBCL) IE A期( Ann Arbor分期)合并同时性早期胃癌且H.pylori阳性的诊治经过.

RNA N 6 -methyladenosine (m 6 A) modifications are essential in plants. Here, we show that transgenic expression of the human RNA demethylase FTO in rice caused a more than threefold increase in grain yield under greenhouse conditions. In field trials, transgenic expression of FTO in rice and potato caused ~50% increases in yield and biomass. We demonstrate that the presence of FTO stimulates root meristem cell proliferation and tiller bud formation and promotes photosynthetic efficiency and drought tolerance but has no effect on mature cell size, shoot meristem cell proliferation, root diameter, plant height or ploidy. FTO mediates substantial m 6 A demethylation (around 7% of demethylation in poly(A) RNA and around 35% decrease of m 6 A in non-ribosomal nuclear RNA) in plant RNA, inducing chromatin openness and transcriptional activation. Therefore, modulation of plant RNA m 6 A methylation is a promising strategy to dramatically improve plant growth and crop yield.

Current endoscopy techniques have difficulties to provide both high resolution and large imaging depth, which significantly hinders the early diagnosis of gastric cancer. Here, we developed a label-free, large-depth, three-dimensional (3D) chromatic reflectance confocal endomicroscopy. In order to solve the problem of insufficient imaging depth of traditional chromatic confocal microscopy, a customized miniature objective lens both with large chromatic focal shift and correction for spherical aberration was used to focus light of different wavelengths at different depths of the sample simultaneously, and a fiber bundle containing 50000 single-mode cores was used to collect the confocal reflectance signal. To acquire detailed information along the axial direction at a faster speed, a high-speed multi-pixel spectrometer was used to realize simultaneous detection of multi-depth signals. Specifically, we have built up a label-free fiber-optic 3D chromatic reflectance confocal endomicroscopy, with 2.3 µm lateral resolution, imaging depth of 570 µm in 3D phantom and 220 µm in tissue, and 1.5 Hz 3D volumetric frame rate. We have demonstrated that the fiber-optic 3D chromatic confocal endomicroscopy can be used to image human gastric tissues ex vivo, and provide important morphological information for diagnosis without labeling. These results show the great potential of the fiber-optic 3D chromatic confocal endomicroscopy for gastric cancer diagnosis.

目的 探讨黏膜内癌和黏膜下层癌在白光内镜下的主要特征.方法 回顾性分析2009年4月～2017年6月我院经内镜黏膜下剥离术(endoscopic submucosal dissection,ESD)或手术切除证实为早期胃癌患者的白光内镜资料,依据术后病理结果将早期胃癌病灶分为黏膜内癌和黏膜下层癌,比较不同病灶间内镜下长径、病灶数目、病灶部位、病灶质地、自发性出血、伴随黏膜色泽、病灶形态和黏膜破损情况等内镜特征.结果 单因素分析显示病灶部位、病灶质地、自发性出血、病灶形态和黏膜破损情况差异有显著性,多因素logistic回归分析显示病灶部位为胃上部(OR =0.538,95％CI:0.394～0.733)、存在自发性出血(OR=2.304,95％CI:1.170～4.537)和病灶形态为凹陷型(OR = 1.374,95％CI:1.016～1.858)是早期胃癌病灶为黏膜下层癌的独立影响因素.结论 早期胃癌病灶中,位于胃上部、有自发性出血的凹陷型病灶,更易浸润黏膜下层.

Background The impact of probiotics on non-Helicobacter pylori gastric microbiota and its role in microbial restoration after eradication were relatively unknown. We aimed to explore the effect of H. pylori eradication and probiotic intervention on gastric microbiota in young adults. Methods Fifty-six H. pylori-negative and 95 H. pylori-positive subjects aged 19-30 were included in this study. H. pylori-infected individuals were randomly assigned to quadruple therapy, probiotics supplemented quadruple therapy, or probiotics monotherapy group. Gastric mucosa and gastric juice samples were collected before and 2 months after treatment for 16SrRNA gene sequencing. Results The gastric microbial community structure and composition differed from H. pylori-negative subjects 2 months after successful H. pylori eradication. The alpha diversity of gastric mucosal microbiota significantly increased and was higher than H. pylori-negative subjects, while the alpha diversity of gastric juice microbiota decreased and was lower than the H. pylori-negative. After probiotics supplemented eradication treatment, Bifidobacterium was enriched in gastric mucosa, Lactobacillus was enriched in gastric juice, potentially pathogenic bacteria such as Fusobacterium and Campylobacter decreased, and the microbial diversity was closer to that of H. pylori-negative subjects compared to quadruple therapy group. Probiotics monotherapy significantly altered the diversity, community structure, and composition of gastric microbiota but showed no advantage in H. pylori inhibition and upregulating beneficial bacteria such as Bifidobacterium and Lactobacillus and related metabolism pathways. Certain potentially pathogenic bacteria such as Fusobacterium increased after probiotic monotherapy. Conclusion H. pylori eradication significantly disrupted gastric microbiota in young adults and could not be restored in a short time. Probiotics supplementation partially helped restore the gastric dysbiosis caused by eradication therapy, but it might be unnecessary for H. pylori-infected young adults to take probiotics alone.

Objective:To evaluate the clinical prognostic significance of molecular markers with high predictive value for lymph node metastasis (LNM) before operation in gastric cancer (GC).Methods:From January 2013 to December 2015, at Peking University Third Hospital, 85 patients with GC confirmed by preoperative biopsy under gastroendoscopy and receiving radical gastrectomy were selected. Among 85 patients with GC, 34 patients had LNM and the other 51 patients were without LNM. The expression levels of macrophage capping protein G (CapG), tyrosine kinase receptor B (TrkB), prosperohomeobox protein l (Prox-1), matrix metalloproteinase-2 (MMP-2), vascular endothelial growth factor-C (VEGF-C) and vascular endothelial growth factor receptor 3 (VEGFR3) were detected by immunohistochemistry (IHC) in preoperative gastric biopsy tissues. Chi-square test was performed to analyze the correlation between the expression of different markers and various clinicopathological characteristics. Receiver operating characteristic (ROC) curve was drawn to compare the predictive value of different markers on LNM of GC. Kaplan-Meier curve was applied to evaluate the impact of different markers on the prognosis of GC patients.Results:The positive expression rates of CapG, TrkB, Prox-1, MMP-2, VEGF-C and VEGFR3 of the LNM-positive group were higher than those of the LNM-negative group (85.3%, 29/34 vs. 35.3%, 18/51; 76.5%, 26/34 vs. 29.4%, 15/51; 67.6%, 23/34 vs. 11.8%, 6/51; 64.7%, 22/34 vs. 33.3%, 17/51; 61.8%, 21/34 vs. 29.4%, 15/51; 52.9%, 18/34 vs. 23.5%, 12/51, respectively), and the differences were statistically significant ( χ2=20.631, 18.093, 28.342, 8.086, 8.746 and 7.727, all P<0.01). The area under the ROC curve (AUC) values and 95% confidence interval ( CI) of CapG, TrkB, Prox-1, MMP-2, VEGF-C and VEGFR3 in predicting LNM of GC before operation were 0.787 (0.687 to 0.880), 0.772 (0.656 to 0.860), 0.761 (0.661 to 0.883), 0.724 (0.618 to 0.830), 0.687 (0.571 to 0.803) and 0.583 (0.452 to 0.715), respectively. Among them, the AUC values of CapG, Prox-1 and TrkB were relatively high. The expression levels of CapG and Prox-1 were correlated with invasion depth and TNM stage of GC ( χ2=4.792, 13.664, 4.204 and 19.948, all P<0.05). And TrkB expression was correlated with TNM stage of GC ( χ2=12.036, P<0.05). Kaplan-Meier curves revealed that the overall survival rates of CapG, TrkB or Prox-1 positive groups were significantly lower than those of CapG, TrkB or Prox-1 negative groups (70.2%, 33/47 vs. 94.7%, 36/38; 70.7%, 29/41 vs. 90.9%, 40/44; 69.0%, 20/29 vs. 87.5%, 49/56, respectively), and the differences were statistically significant ( χ2=9.820, 4.909 and 4.683, all P<0.05). Conclusions:CapG, TrkB and Prox-1 are markers with relatively high predictive value for LNM of GC, and all of them are correlated with the progression and poor prognosis of GC.

Research on N6-methyladenosine (m6A) in recent years has revealed the complex but elegant regulatory role of this RNA modification in multiple physiological processes. The advent of m6A detection technologies is the basis for studying the function of this RNA modification. These technologies enable the detection of m6A sites across transcriptome or at specific gene, thereby revealing the alternation and dynamic of RNA modification. However, non-specific signals that arise from the antibody-based methods and the low-resolution landscape have become the major drawback of classic m6A detection methods. In this review, we summarize the current available methods and categorized them into three groups according to the utilization purpose, including measurement of total m6A levels, detection m6A locus in single gene, and m6A sequencing. We hope this review helps researchers in epitranscriptomic field find an appropriate m6A detection tool that suites their experimental design.