Publications by authors named "Zhonghua Du"

Background: B-cell prolymphocytic leukemia (B-PLL) is a rare mature B-cell tumor with an aggressive clinical course and poor prognosis. It is characterized by prominent splenomegaly and prolymphocytes exceeding 55% of the lymphoid cells in the blood. Purine analog-based chemo-immunotherapy is the first-line therapy for B-PLL.

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In order to adapt to the launch velocity of modern artillery, it is necessary to study the fracture mechanism of the high-velocity penetration of penetrators. Therefore, the penetration fracture mode of tungsten-fiber-reinforced Zr-based bulk metallic glass matrix composite (WF/Zr-MG) rods at a high velocity is studied. An experiment on WF/Zr-MG rods penetrating into rolled homogeneous armor steel (RHA) was carried out at 1470~1650 m/s.

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Rationale: Poor graft function (PGF) occurs in 5% to 27% of allogeneic hematopoietic stem cell transplantation (allo-HSCT) and is associated with high life-threatening complications. The etiology of PGF is complex and multifactorial, and iron overload (IOL) is considered as a predictive factor.

Patient Concern: A 45-years-old woman who was diagnosed as low-risk myelodysplastic syndrome in 2012 has been transfusion dependent and developed severe IOL.

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This paper aims to study the penetration effect of harpoons on space debris to ensure the sustainable development of the space environment and solve the increasingly serious space debris problem. Firstly, a harpoon system was designed to capture space debris. Secondly, based on the Johnson-Cook dynamic constitutive model and fracture failure criterion, the finite element models of aluminum alloy plates were established.

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Nuclear reprogramming of somatic cells into a pluripotent status has the potential to create patient-specific induced pluripotent stem cells for regenerative medicine. Currently, however, the epigenetic mechanisms underlying this pluripotent reprogramming are poorly understood. To delineate this epigenetic regulatory network, we utilized a chromatin RNA in situ reverse transcription sequencing (CRIST-seq) approach to identify long noncoding RNAs (lncRNAs) embedded in the 3-dimensional intrachromosomal architecture of stem cell core factor genes.

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The space harpoon is a rigid-flexible, coupled debris capture method with a simple, reliable structure and a high adaptability to the target. For the process of impacting and embedding the harpoon into the target plate, the effect of friction at a low-velocity impact is studied, and the criteria for effective embedding of the harpoon and the corresponding launch velocity are determined. A simulation model of the dynamics of the harpoon and the target plate considering tangential friction is established, and the reliability of the numerical simulation model is verified by comparing the impact test, focusing on the kinetic energy change and embedding length during the impact of the harpoon.

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The liner is an important part of shaped charge. In this paper, the spherical cone composite structure liner composed of a spherical missing body and truncated cone (hereinafter referred to as the SCS liner) is studied. The SCS liner is made of copper.

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The molecular circuitry that causes stem cells to exit from pluripotency remains largely uncharacterized. Using chromatin RNA in situ reverse transcription sequencing, we identified Peln1 as a novel chromatin RNA component in the promoter complex of Oct4, a stem cell master transcription factor gene. Peln1 was negatively associated with pluripotent status during somatic reprogramming.

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Background: A specific 3-dimensional intrachromosomal architecture of core stem cell factor genes is required to reprogram a somatic cell into pluripotency. As little is known about the epigenetic readers that orchestrate this architectural remodeling, we used a novel chromatin RNA in situ reverse transcription sequencing (CRIST-seq) approach to profile long noncoding RNAs (lncRNAs) in the Oct4 promoter.

Results: We identify Platr10 as an Oct4 - Sox2 binding lncRNA that is activated in somatic cell reprogramming.

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This study was to investigate clinical features and prognosis of duplex primary malignant neoplasms involving chronic myeloid leukemia (CML-DPMNs). Clinical data of thirteen CML-DPMN patients who were admitted to the First Hospital of Jilin University from May 2008 to December 2018 were collected and retrospectively analyzed. Female patients (9/13) were predominant in this cohort study.

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Background: Hepatosplenic T-cell lymphoma (HSTCL) is a rare subtype of non-Hodgkin's lymphoma, which has an aggressive clinical course and an extremely poor prognosis. Chidamide is a novel, orally active, benzamide-type histone deacetylase (HDAC) inhibitor that has been used for peripheral T-cell lymphoma (PTCL) treatment. However, to date, there has been no report of the treatment and effect of the HDAC inhibitor chidamide in HSTCL, which is a special subtype of PTCL.

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Based on mechanical properties of Polyamide 66 (PA66) under complex loading conditions, a Drucker-Prager yield criterion was employed to characterize its yield behavior. Then, a one-dimensional model, which contains a viscoelastic regime and a viscoplastic regime, was introduced and converted into a three-dimensional constitutive model. The three-dimensional model was implemented into a LS-DYNA software, which was used to predict the dynamic response of PA66 under Taylor impact conditions, whose corresponding tests were conducted by gas gun and recorded by high-speed camera.

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Induced pluripotent stem cells (iPSCs), derived from reprogramming of somatic cells by a cocktail of transcription factors, have the capacity for unlimited self-renewal and the ability to differentiate into all of cell types present in the body. iPSCs may have therapeutic potential in regenerative medicine, replacing injured tissues or even whole organs. In this study, we examine epigenetic factors embedded in the specific 3-dimensional intrachromosomal architecture required for the activation of endogenous pluripotency genes.

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Background: Sjögren syndrome (SS) is a chronic and systemic autoimmune disease characterized by lymphocytic infiltration of the exocrine glands. And histoplasmosis is an invasive mycosis caused by the saprophytic dimorphic fungus . In patients with primary SS (PSS), disseminated histoplasmosis (DH) is extremely rare.

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The fusion product of FIP1-like-1 (FIP1L1) and platelet-derived growth factor receptor α (PDGFRA) gene rearrangement is a tyrosine kinase oncoprotein sensitive to imatinib. This gene rearrangement characterizes a novel clinico-biological class of myeloid and lymphoid neoplasms with eosinophilia and PDGFRA abnormalities. The DEK proto-oncogene (DEK) and nucleoporin 214 (NUP214) rearrangement is rare in patients with acute myeloid leukemia (AML); therefore, the coexistence of DEK-NUP214 and FIP1L1-PDGFRA rearrangements in patients with AML is extremely rare.

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Formation of a pluripotency-specific chromatin network is a critical event in reprogramming somatic cells into pluripotent status. To characterize the regulatory components in this process, we used 'chromatin RNA in situ reverse transcription sequencing' (CRIST-seq) to profile RNA components that interact with the pluripotency master gene Oct4. Using this approach, we identified a novel nuclear lncRNA Oplr16 that was closely involved in the initiation of reprogramming.

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Rationale: Concurrent calreticulin (CALR) mutation and BCR-ABL1 fusion are extremely rare in chronic myelogenous leukemia; to date, only 12 cases have been reported.

Patient Concerns: A 57-year-old male who had an 11-year history of essential thrombocytosis presented to our hospital with leukocytosis and marked splenomegaly for 3 months.

Diagnoses: Chronic myelogenous leukemia with myeloid fibrosis arising on the background of essential thrombocytosis harboring both BCR-ABL1 fusion and type-1 like CALR mutation.

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Long non-coding RNAs (lncRNAs) constitute an important component of the regulatory apparatus that controls stem cell pluripotency. However, the specific mechanisms utilized by these lncRNAs in the control of pluripotency are not fully characterized. We utilized a RNA reverse transcription-associated trap sequencing (RAT-seq) approach to profile the mouse genome-wide interaction targets for lncRNAs that are screened by RNA-seq.

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Natural killer (NK)-based immunotherapeutic strategies are showing promise in the clinic, particularly against acute myeloid leukemia (AML). Similar treatments for T-cell acute lymphoblastic leukemia (T-ALL) have been less successful, which is due to the higher resistance of T-ALL blasts to the cytotoxic function of NK cells. Herein, microRNA-29b (miR-29b) upregulation was identified in NK cells in both neurogenic locus notch homolog protein 1 (Notch1)-T-ALL mice and patients with T-ALL.

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Long noncoding RNAs (lncRNAs) can regulate the activity of target genes by participating in the organization of chromatin architecture. We have devised a "chromatin-RNA in situ reverse transcription sequencing" (CRIST-seq) approach to profile the lncRNA interaction network in gene regulatory elements by combining the simplicity of RNA biotin labeling with the specificity of the CRISPR/Cas9 system. Using gene-specific gRNAs, we describe a pluripotency-specific lncRNA interacting network in the promoters of and , two critical stem cell factors that are required for the maintenance of pluripotency.

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Background: Friend leukemia virus integration 1 (FLI1), an ETS transcription factor family member, acts as an oncogenic driver in hematological malignancies and promotes tumor growth in solid tumors. However, little is known about the mechanisms underlying the activation of this proto-oncogene in tumors.

Results: Immunohistochemical staining showed that FLI1 is aberrantly overexpressed in advanced stage and metastatic breast cancers.

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Pluripotent stem cells hold great investigative potential for developmental biology and regenerative medicine. Recent studies suggest that long noncoding RNAs (lncRNAs) may function as key regulators of the maintenance and the lineage differentiation of stem cells. However, the underlying mechanisms by which lncRNAs affect the reprogramming process of somatic cells into pluripotent cells remain largely unknown.

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Aberrant insulin-like growth factor I receptor (IGF1R) signaling pathway serves as a well-established target for cancer drug therapy. The intragenic antisense long noncoding RNA (lncRNA) IRAIN, a putative tumor suppressor, is downregulated in breast cancer cells, while IGF1R is overexpressed, leading to an abnormal IGF1R/IRAIN ratio that promotes tumor growth. To precisely target this pathway, we developed an "antisense lncRNA-mediated intragenic cis competition" (ALIC) approach to therapeutically correct the elevated IGF1R/IRAIN bias in breast cancer cells.

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