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We present a facile strategy to achieve purely organic multi-colour room-temperature phosphorescence (RTP) films by doping typical fused-ring compounds into a poly(vinyl alcohol) matrix. Such RTP films demonstrate inherent RTP emission ranging from green to red with a long lifetime and high quantum yield (QY) (lifetime: ∼0.56 ms, QY: ∼35.4%). We further exploit such high-performance RTP films for dynamic information encryption. [ABSTRACT FROM AUTHOR]

We report the "water‐in‐oil‐in‐water" preparation of kidney injury molecule‐1‐targeting supramolecular chemiluminescence (CL) reporters (PCCS), consisting of L‐serine‐modified poly(lactic‐co‐glycolic) acid (PLGA)‐encapsulated peroxyoxalate (CPPO), chlorin e6 (Ce6) and superoxide dismutase (SOD), for early diagnosis and amelioration of acute kidney injury (AKI). In this system, O2⋅−, a biomarker of AKI, triggers the oxidation of CPPO to 1,2‐dioxetanedione and subsequent CL emission via CL resonance energy transfer to Ce6. The L‐serine‐modified PLGA stabilizes CPPO and Ce6 via noncovalent interactions, promoting long‐lived CL (half‐lives: ≈1000 s). Transcriptomics analysis shows that PCCS reporters reduce the inflammatory response through glutathione metabolism and inhibition of the tumor necrosis factor signaling pathway. The reporters are able to non‐invasively detect AKI at least 12 h earlier than current assays, and their antioxidant properties allow simultaneous treatment of AKI. [ABSTRACT FROM AUTHOR]

We report the "water‐in‐oil‐in‐water" preparation of kidney injury molecule‐1‐targeting supramolecular chemiluminescence (CL) reporters (PCCS), consisting of L‐serine‐modified poly(lactic‐co‐glycolic) acid (PLGA)‐encapsulated peroxyoxalate (CPPO), chlorin e6 (Ce6) and superoxide dismutase (SOD), for early diagnosis and amelioration of acute kidney injury (AKI). In this system, O2⋅−, a biomarker of AKI, triggers the oxidation of CPPO to 1,2‐dioxetanedione and subsequent CL emission via CL resonance energy transfer to Ce6. The L‐serine‐modified PLGA stabilizes CPPO and Ce6 via noncovalent interactions, promoting long‐lived CL (half‐lives: ≈1000 s). Transcriptomics analysis shows that PCCS reporters reduce the inflammatory response through glutathione metabolism and inhibition of the tumor necrosis factor signaling pathway. The reporters are able to non‐invasively detect AKI at least 12 h earlier than current assays, and their antioxidant properties allow simultaneous treatment of AKI. [ABSTRACT FROM AUTHOR]

We have identified a variant on the β-globin gene in a Chinese female. Sequencing of the HBB gene revealed a Phe→Leu substitution at codon 42[β42(CD1) Phe→Leu, HBB:c.129T > A] which has been named Hb Suqian for where the proband was born. [ABSTRACT FROM AUTHOR]

I DDX41 i mutations were detected in 0.6% (2/329) adult ALL patients of our cohorts comparable with a recent report.[10] Previous studies showed that I DDX41 i -mutated patients of MNs presented as male predominance and old age. Germline DDX41 mutations define a significant entity within adult MDS/AML patients. We found three variants in I DDX41 i (p.R525H, p.G530D and p.Y259C) and confirmed the germline origin of p.Y259C of I DDX41 i by Sanger sequencing. [Extracted from the article]

We retrospectively explored the prognostic impact of DAT mutations at diagnosis in 122 RUNX1mut AML patients. RUNX1 missense mutation was dominant in the RUNT domain, and frameshift mutation was dominant in the TAD domain. DAT mutations occurred in 38.5% of RUNX1mut AML. After propensity score matching, DATpos patients had worse two-year relapse-free survival (RFS) than DATneg patients (p =.041). Moreover, RUNX1high (VAF ≥ 37.6%) patients showed poorer two-year overall survival (OS) and RFS than RUNX1low (VAF < 37.6%) patients (OS, p =.033; RFS, p =.027), especially in the RUNX1highDATpos group. Additionally, multivariate analysis confirmed that DAT mutations at diagnosis were an independent adverse factor for RFS. There were no significant differences in two-year OS and RFS between DATpos and DATneg patients or between RUNX1high and RUNX1low patients who undergoing allogeneic hematopoietic stem cell transplantation (allo-HSCT). Collectively, DAT mutations at diagnosis were adverse factors for RFS, and allo-HSCT could likely improve the poor outcomes of these patients. [ABSTRACT FROM AUTHOR]

Background: High‐grade intraepithelial neoplasia (HIN) is the precursor of oesophageal squamous cell carcinoma. The molecular and functional properties of HIN are determined by intrinsic origin cells and the extrinsic microenvironment. Yet, these factors are poorly understood. Methods: We performed single‐cell RNA sequencing of cells from HINs and adjacent tissues from the human oesophagus. We analysed the heterogeneity of basal layer cells and confirmed it using immunostaining. Aneuploid cells in HIN were studied using primary cell culture combined with karyotype analysis. We reconstructed the lineage relationship between tumour and normal populations based on transcriptome similarity. Integration analysis was applied to our epithelial data and published invasive cancer data, and results were confirmed by immunostaining and 3D organoid functional experiments. We also analysed the tumour microenvironment of HIN. Results: The basal layer contained two cell populations: KRT15highSTMN1low and KRT15highSTMN1high cells, which were located mainly in the interpapillary and papillary zones, respectively. The KRT15highSTMN1low population more closely resembled stem cells and transcriptome similarity revealed that HIN probably originated from these slow‐cycling KRT15highSTMN1low cells. 3D Organoid experiments and RNA‐sequencing showed that basal‐cell features and the differentiation ability of the normal epithelium were largely retained in HIN, but may change dramatically in tumour invasion stage. Moreover, the tumour microenvironment of HIN was characterised by both inflammation and immunosuppression. Conclusions: Our study provides a comprehensive single‐cell transcriptome landscape of human oesophageal HIN. Our findings on the origin cells and unique microenvironment of HIN will allow for the development of strategies to block tumour progression and even prevent cancer initiation. [ABSTRACT FROM AUTHOR]

Most clinical characteristics of MDS/AML patients with variants in the SWI/SNF complex were similarly distributed as those in patients with wild-type genes (Table I). Keywords: SWI/SNF; mutation; acute myeloid leukaemia; myelodysplastic syndrome; prognosis EN SWI/SNF mutation acute myeloid leukaemia myelodysplastic syndrome prognosis 441 444 4 01/17/22 20220115 NES 220115 Myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML) are heterogeneous groups of myeloid neoplasms. In the present study, we analyzed the frequency, clinical and prognostic significance of mutations in 29 genes encoding SWI/SNF complex in MDS/AML patients. Considering all variants in the SWI/SNF complex as one group, overall survival (OS) was significantly longer in the presence of SWI/SNF variants [Hazard ratio (HR) 0-38, 95% CI 0-202-0-704; I P i = 0-027; Fig 1C]. [Extracted from the article]