Publications by authors named "Shenglai Li"

Objective: Hereditary hemochromatosis (HH) is a common genetic disorder characterized by iron overload, which, if undiagnosed, can lead to severe organ damage. There are 4 types of HH. Type 1 HH, the most common form, is primarily caused by a common variant in Western Europe (p.

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Background: Anxiety is common preceding tooth extraction; hence, it is crucial to identify patients with dental anxiety (DA) and to manage DA. This study assessed the level of DA and influencing factors in tooth extraction patients in a dental hospital in China and changes in their blood pressure (BP) and heart rate (HR) during the tooth-extraction procedure.

Methods: The study was a cohort study.

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The production of vanillin from biomass offers a sustainable route for synthesizing daily-use chemicals. However, achieving sunlight-driven vanillin synthesis through HO activation in an aqueous environment poses challenges due to the high barrier of HO dissociation. In this study, we have successfully developed an efficient approach for gram-scale vanillin synthesis in an aqueous reaction, employing Mn-defected γ-MnO as a photocatalyst at room temperature.

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: To assess the () recombinant gingivalis gingipain R2 (rRgpB)-induced Ca mobilization in human gingival fibroblast (HGF) mediated by protease-activated receptor (PAR) and its downstream signal transduction pathways. : Flow cytometry was used to detect the expression of PAR in HGF. The proliferation of HGF was measured by CCK-8.

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The goal of the National Cancer Institute's (NCI's) Genomic Data Commons (GDC) is to provide the cancer research community with a data repository of uniformly processed genomic and associated clinical data that enables data sharing and collaborative analysis in the support of precision medicine. The initial GDC dataset include genomic, epigenomic, proteomic, clinical and other data from the NCI TCGA and TARGET programs. Data production for the GDC started in June, 2015 using an OpenStack-based private cloud.

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Arginine-specific cysteine proteinases, such as Arg-gingipain B (RgpB), mediate inflammation by activating protease-activated receptors (PARs). Arg-gingipain B is produced by Porphyromonas gingivalis, and is implicated in the causation of periodontal disease. The purpose of the present study was to observe the influence of recombinant RgpB protein (rRgpB) on PAR activation by monitoring intracellular Ca2+ ion concentration ([Ca2+]i) and inositol-1,4,5-triphosphate (IP3) levels in human gingival fibroblasts (HGFs).

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Severe malocclusion can contribute to several serious dental and physical conditions, such as digestive difficulties, periodontal disease, and severe tooth decay. Orthodontic treatment is mainly used to treat malocclusion. Forces in orthodontic tooth results in bone resorption on the pressure side and bone deposition on the tension side.

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N-Methyladenosine (mA) represents the most prevalent internal modification in mammalian mRNAs. Despite its functional importance in various fundamental bioprocesses, the studies of mA in cancer have been limited. Here we show that FTO, as an mA demethylase, plays a critical oncogenic role in acute myeloid leukemia (AML).

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Acute myeloid leukemia (AML) is a common and fatal form of hematopoietic malignancy. Overexpression and/or mutations of FLT3 have been shown to occur in the majority of cases of AML. Our analysis of a large-scale AML patient cohort (N = 562) indicates that FLT3 is particularly highly expressed in some subtypes of AML, such as AML with t(11q23)/MLL-rearrangements or FLT3-ITD.

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Article Synopsis
  • * Increasing miR-22 levels in leukemia cells decreases their growth and conservatively impedes the progression of the disease in experimental models, indicating its potential therapeutic application.
  • * The study identifies a complex signaling circuit involving TET1, GFI1, EZH2, SIN3A, and miR-22 that contributes to the regulation of leukemia-promoting pathways, shedding light on the genetic and epigenetic factors driving AML and the possibilities for mi
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Expression of functionally important genes is often tightly regulated at both transcriptional and post-transcriptional levels. We reported previously that TET1, the founding member of the TET methylcytosine dioxygenase family, plays an essential oncogenic role in MLL-rearranged acute myeloid leukemia (AML), where it is overexpressed owing to MLL-fusion-mediated direct up-regulation at the transcriptional level. Here we show that the overexpression of TET1 in MLL-rearranged AML also relies on the down-regulation of miR-26a, which directly negatively regulates TET1 expression at the post-transcriptional level.

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Overexpression of HOXA/MEIS1/PBX3 homeobox genes is the hallmark of mixed lineage leukemia (MLL)-rearranged acute myeloid leukemia (AML). HOXA9 and MEIS1 are considered to be the most critical targets of MLL fusions and their coexpression rapidly induces AML. MEIS1 and PBX3 are not individually able to transform cells and were therefore hypothesized to function as cofactors of HOXA9.

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Background: Protease-activated receptors (PARs) are G-protein-coupled receptors with an active role in mediating inflammation, pain and other functions. The oral pathogen Porphyromonas gingivalis (P. gingivalis) secretes proteases that activate PARs.

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It is generally assumed that gain- and loss-of-function manipulations of a functionally important gene should lead to the opposite phenotypes. We show in this study that both overexpression and knockout of microRNA (miR)-126 surprisingly result in enhanced leukemogenesis in cooperation with the t(8;21) fusion genes AML1-ETO/RUNX1-RUNX1T1 and AML1-ETO9a (a potent oncogenic isoform of AML1-ETO). In accordance with our observation that increased expression of miR-126 is associated with unfavorable survival in patients with t(8;21) acute myeloid leukemia (AML), we show that miR-126 overexpression exhibits a stronger effect on long-term survival and progression of AML1-ETO9a-mediated leukemia stem cells/leukemia initiating cells (LSCs/LICs) in mice than does miR-126 knockout.

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Objective: To investigate the expression types of protease-activated receptors(PAR) in human gingival fibroblasts(HGF) and the functions of PAR in periodontitis.

Methods: Primary HGF were cultured.Reverse transcription PCR(RT-PCR) was used to detect the expression of PAR in HGF.

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Objective: Protease-activated receptors (PARs) are a unique class of receptors which are implicated in mediating inflammation, pain and other functions. The aim of this study was to elucidate the role of PARs in the pathogenesis of chronic periodontitis by differential expression analysis of PARs in the gingival tissues of chronic periodontitis patients compared with those of healthy control individuals.

Design: Gingival tissue specimens were collected from chronic periodontitis patients (n=20) and control individuals (n=20).

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Background: A lipoma is a benign tumor which may occur in the adipose tissue of any part of the body. The tumor is most commonly found on the trunk and extremities. Although it is the most common tumor of mesenchymal origin in the head and neck, its incidence is relatively rare.

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A new peptide scaffold was made by mixing pure RADA16 (Ac-RADARADARADARADA-CONH2) and designer peptide RGDA16 (Ac-RADARGDARADARGDA-CONH2) solutions, and investigate any effect on attachment, spreading and proliferation of pre-osteoblast (MC3T3-E1). The peptides, RADA16 and RGDA16, were custom-synthesized. They were solubilized in deionized water at a concentration of 10 mg/ml (1% w/v), the RGDA16 peptide solution was mixed 1:1 with RADA16 solution and a new peptide solution RGDAmix was produced.

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Lipopolysaccharide (LPS) derived from the periodontal pathogen Porphyromonas gingivalis has been shown to differ from enterobacterial LPS in structure and function; therefore, the Toll-like receptors (TLRs) and the intracellular inflammatory signaling pathways are accordingly different. To elucidate the signal transduction pathway of P. gingivalis, LPS-induced pro-inflammatory cytokine production in the human monocytic cell line THP-1 was measured by ELISA, and the TLRs were determined by the blocking test using anti-TLRs antibodies.

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