Publications by authors named "Keqi Han"

The development of titanium alloys is limited by issues such as low hardness, poor wear resistance, and sensitivity to adhesive wear. Using laser cladding technology to create high-hardness wear-resistant coatings on the surface of titanium alloys is an economical and efficient method that can enhance their surface hardness and wear resistance. This paper presents the preparation of two types of nickel-based composite coatings, Ni60-Ti-Cu-xBC and Ni60-Ti-Cu-BC-xCeO, on the surface of TC4 titanium alloy using laser cladding.

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CTCF plays an important role in 3D genome organization by adjusting the strength of chromatin insulation at TAD boundaries, where clustered CBS (CTCF-binding site) elements are often arranged in a tandem array with a complex divergent or convergent orientation. Here, using Pcdh and HOXD loci as a paradigm, we look into the clustered CTCF TAD boundaries and find that, counterintuitively, outward-oriented CBS elements are crucial for inward enhancer-promoter interactions as well as for gene regulation. Specifically, by combinatorial deletions of a series of putative enhancer elements in mice in vivo or CBS elements in cultured cells in vitro, in conjunction with chromosome conformation capture and RNA-seq analyses, we show that deletions of outward-oriented CBS elements weaken the strength of long-distance intra-TAD promoter-enhancer interactions and enhancer activation of target genes.

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Background: Although checkpoint blockade is a promising approach for the treatment of hepatocellular carcinoma (HCC), subsets of patients expected to show a response have not been established. As T cell-mediated tumor killing (TTK) is the fundamental principle of immune checkpoint inhibitor therapy, we established subtypes based on genes related to the sensitivity to TKK and evaluated their prognostic value for HCC immunotherapies.

Methods: Genes regulating the sensitivity of tumor cells to T cell-mediated killing (referred to as GSTTKs) showing differential expression in HCC and correlations with prognosis were identified by high-throughput screening assays.

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The purpose of this study was to screen for changes in chemokine and chemokine-related genes that are expressed in hepatocellular carcinoma (HCC) as potential markers of HCC progression. Total RNA was extracted from tumor and peritumor tissues from mice with HCC and analyzed using a PCR microarray comprising 98 genes. Changes in gene expression of threefold or more were screened and subsequently confirmed by immunohistochemical analyses and western blotting.

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Hepatocellular carcinoma (HCC) is an aggressive malignancy and a major cause of cancer-related mortality worldwide. Our previous study shows that chemokine (C-X-C motif) ligand 1 (CXCL1) was upregulated and CXCR1 was downregulated in tumor tissues as compared to peritumor tissues by chemotaxis assay. As the status of CXCL subgroups and their receptors affect progression of HCC, we evaluated potential mechanisms of CXCL1 associated with anticancer effects in HCC based on our previous study.

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Aim: To study the inflammatory microenvironment and expression of chemokines in hepatocellular carcinoma (HCC) in nude mice.

Methods: CBRH-7919 HCC cells were injected into the subcutaneous region of nude mice. Beginning two weeks after the challenge, tumor growth was measured every week for six weeks.

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Introduction: We report outcomes for a phase II study of the combination of weekly docetaxel and cisplatin in elderly patients with advanced non-small cell lung cancer.

Methods: Patients with chemotherapy-naive, stage IIIB/IV, an Eastern Cooperative Oncology Group performance status of 0 or 1, ages 70 years or older, were eligible. Chemotherapy consisted of cisplatin (25 mg/m2) on days 1, 8, and 15 and docetaxel (20 mg/m2) on days 1, 8, and 15 every 4 weeks.

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Objective: Diagnosis of lung cancer at an early disease stage is important for successful treatment and improving the outcome of patients. To improve its prognosis, we attempted to explore novel tools for screening serum biomarkers to distinguish lung cancer from healthy individuals by serum protein profiles and a classification tree algorithm.

Methods: Serum samples were applied to metal affinity protein chips to generate mass spectra by surface-enhanced laser desorption/ionization (SELDI) time-of-flight mass spectrometry.

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Aim: To investigate anti-tumor activities and apoptosis-regulated mechanisms of bufalin in the orthotopic transplantation tumor model of human hepatocellular carcinoma in nude mice.

Methods: BEL-7402 cells of human hepatocellular carcinoma were inoculated to form subcutaneous tumors, and were implanted into the liver to establish orthotopic transplantation tumor models of human hepatocellular carcinoma in nude mice. Seventy-five animals were randomized divided into five groups (n = 15).

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Objective: To investigate the anti-tumor effect of bufalin and its regulation on Bcl-2 and Bax proteins in orthotopically transplanted tumor of human hepatocellular carcinoma in nude mice.

Methods: Orthotopically transplanted tumor of human hepatocellular carcinoma was established in nude mice. The mice were randomly divided into five groups: high-dose bufalin-treated group (1.

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Objective: The aim of this study was to investigate the cellular effects of melittin on the growth and apoptosis of human hepatocellular carcinoma (HCC) cells and to provide the molecular mechanism for potential application of a recombinant adenovirus carrying the melittin gene (Ad-rAFP-Mel) in the treatment of liver cancer.

Methods: Human HCC cells (BEL-7402) were infected with Ad-rAFPMel at different times. In vitro cell growth was determined by MTT assay.

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Objective: To study the feasibility of the establishment of the orthotopic transplantation tumor model of hepatocellular carcinoma in mice and its tumor biological characteristics.

Methods: H22 cells of hepatocellular carcinoma were inoculated to form ectopic transplanted model in mice by subcutaneous injection. Then the subcutaneous tumors were implanted into the liver of mice, and the orthotopic transplantation tumor model of hepatocellular carcinoma was established.

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