Publications by authors named "Zhi-an Zhu"

Materials with spin dimers have attracted much attention in the last several decades because they could provide a playground to embody simple quantum spin models. For example, the Bose-Einstein condensation of magnons has been observed in TlCuCl with anti-ferromagnetic CuCl dimers. In this work, we have synthesized a new kind of single-crystal LiRbGdTeO with GdO dimers.

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Special AT-rich-sequence-binding protein 1 (SATB1), a new type of gene regulator, has been reported to be expressed in various human cancers and may be associated with malignancy. The aim of this study was to investigate the expression of SATB1 in astrocytoma and to determine its prognostic value for the overall survival of patients with astrocytoma. The expression of SATB1 protein and messenger RNA (mRNA) in human astrocytoma specimens was examined using immunohistochemistry and semi-quantitative reverse transcription polymerase chain reaction (RT-PCR).

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Previous studies showed that solute carrier family 22 member 18 (SLC22A18) is involved in tumorigenesis. The aim of this study was to examine the role of SLC22A18 in glioma cells. Glioma U251 cells were transfected with the human SLC22A18 gene.

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Article Synopsis
  • The study investigates the role of SATB1, a protein linked to various human cancers, in gliomas, focusing on its expression levels, associations with cancer aggressiveness, and potential impacts on patient survival.
  • Researchers found that SATB1 was expressed in 62.9% of glioma tumors and correlated with higher tumor grades, increased cell proliferation (Ki67), and poorer patient outcomes, while showing an inverse relationship with MGMT promoter methylation.
  • In laboratory tests, reducing SATB1 expression in U251 glioma cells led to decreased growth, invasion, and new blood vessel formation, while promoting cell death, suggesting SATB1 might be a crucial factor in glioma progression and a potential target for therapy.
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We investigated the expression of the putative tumor suppressor SLC22A18 to evaluate it as a prognostic marker in glioma patients. Immunohistochemical and Western blot analyses of clinical tissue samples obtained from 120 patients with glioma were performed. Low expression of SLC22A18 was observed in 71.

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SLC22A18 [solute carrier family 22 (organic cation transporter) member 18] is located within the 11p15.5 cluster, and may be a new tumor suppressor gene; evidence of SLC22A18 hypermethylation is documented in several types of human cancers. In order to determine whether SLC22A18 hypermethylation is involved in glioma, we determined the SLC22A18 gene protein expression, mRNA expression and methylation status in glioma U251 cells before and after treatment with 5-Aza-2'‑deoxycytidine (5-Aza-CdR), and observed the change in growth.

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Background: Downregulation of the putative tumor suppressor gene SLC22A18 has been reported in a number of human cancers. The aim of this study was to investigate the relationship between SLC22A18 downregulation, promoter methylation and the development and progression of human glioma.

Method: SLC22A18 expression and promoter methylation was examined in human gliomas and the adjacent normal tissues.

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The hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) are important cytokines with modulatory actions in the nervous system. The present study aimed to investigate the role and expression of HGF and VEGF in the cerebral tissue of adult rats with chronic hydrocephalus after subarachnoid hemorrhage. Adult female Wistar rats were randomly divided into 4 groups: a control group (n=20) and 3 experimental subgroups (n=60).

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Cell culture, tissue chemistry and flow cytometry were used to determine whether antisense c-Met oligodeoxynucleotides enhanced the sensitivity of human glioma cells to paclitaxel. A combination of paclitaxel with antisense c-Met oligodeoxynucleotides inhibited cell growth, induced apoptosis and induced c-Met protein expression in U251 and SHG44 human glioma cells more significantly than either paclitaxel or the oligodeoxynucleotides on their own (P<0.01).

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Article Synopsis
  • * The study utilized RNA interference (RNAi) to create shRNA vectors specifically targeting the c-Met gene in glioma U251 cells, significantly reducing c-Met expression by up to 90%.
  • * Results showed that inhibiting c-Met led to decreased growth and metastasis of U251 cells and increased apoptosis, suggesting RNAi targeting of c-Met could be an effective strategy for antiangiogenic cancer therapies.
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Hypoxia regulates expression of hepatocyte growth factor (HGF) by increasing its transcription and by stabilizing its mRNA. Despite the pivotal role of hypoxia-inducible factor 1 (HIF-1) in transcriptional activation of hypoxia-responsive genes, it is not known whether HIF-1 mediates hypoxia-induced stabilization of HGF mRNA. We constructed adenoviral vectors expressing either the wild-type HIF-1alpha (Ad2/HIF-1alpha/FL), a constitutively stable hybrid form of HIF-1alpha (Ad2/HIF-1alpha/VP16), or no transgene (Ad2/CMVEV).

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Article Synopsis
  • Postoperative radiotherapy is the usual treatment for patients with a type of brain tumor called malignant glioma, but these tumors often come back because they resist radiation.
  • The study looked at how three different glioma cell lines reacted to radiation and measured a special protein called HGF, which is linked to tumor growth and survival.
  • The results showed that higher radiation doses increased HGF levels in all cell lines, but one specific cell line (BT325) had much more HGF and was harder to kill with radiation, suggesting it could grow back even after treatment.
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Background: c-Met, a receptor tyrosine kinase, and its ligand, hepatocyte growth factor, are critical in cellular proliferation, motility, and invasion and are known to be overexpressed in gliomas. The aim of our study was to investigate the uptake and effects of c-Met antisense oligodeoxynucleotides (ASODNs) on rat and human glioma cells in vitro and the uptake and toxicity of these nucleotides in rat carcinomatosis and brain tumor models.

Materials And Methods: The three human cell lines (U87, BT325, SHG44) and the C6 rat glioma cell line were cultured.

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Hepatocyte growth factor (HGF) is a pleiotrophic cytokine that stimulates motility and invasion of several cancer cell types and induces angiogenesis, which is known to be expressed in several malignancies including glioma. The effect of transforming growth factor-beta (TGF-beta) isoforrns as well as gangliosides on HGF production was investigated in human glioma cell lines. TGF-beta isoforms and gangliosides were found to differentially stimulate HGF production by these cells.

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C-Met, a receptor tyrosine kinase, and its ligand, hepatocyte growth factor (HGF), are critical in cellular proliferation, motility, and invasion, and are known to be overexpressed in gliomas, which are related to the repair of damaged DNA. In this study, we investigated both in vitro and in vivo whether inhibition of the c-Met gene by antisense oligonucleotides (ODNs) enhances the cytotoxic effect of radiation on human U251 gliomas. A volume of 100 nM of c-Met antisense ODNs inhibited the level of mRNA by more than 95% and reduced the protein expression by about 70%.

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Objective: To evaluate the change in Fas antigen expression and apoptosis of neurons, to provide an experimental evidence of loss of neurons in craniocerebral injury, and to provide experimental evidence for clarifying multi-approach of the lost neuron after damage.

Methods: Brain impact injury was reproduced in SD rat with a free falling impacting device. Using immunohistochemistry method the Fas protein expression was assessed and apoptotic cells were detected with electron microscopy.

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Objective: To investigate the effects of magnesium sulfate on traumatic brain edema and explore its possible mechanism.

Methods: Forty-eight Sprague-Dawley (SD) rats were randomly divided into three groups: Control, Trauma and Treatment groups. In Treatment group, magnesium sulfate was intraperitoneally administered immediately after the induction of brain trauma.

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