Publications by authors named "Ji Li-Juan"

Article Synopsis
  • Hepatocellular carcinoma (HCC) is a highly malignant liver tumor with low survival rates, and the study focuses on the role of the FITM2 gene in lipid metabolism and HCC progression.* -
  • Researchers found that FITM2 is highly expressed in HCC tissues, correlating with worse outcomes like microvascular invasion and reduced survival rates.* -
  • Experiments showed that reducing FITM2 expression inhibits HCC cell migration by affecting caveolin-1 and caveolae formation, suggesting FITM2 as a potential target for new therapies.*
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Background: Proteomics analysis may provide important information regarding the pathogenesis of chronic myofascial pain and the mechanisms underlying the treatment effects of dry needling.

Materials And Methods: This study used a rat model of myofascial trigger points (MTrPs) to perform a proteomics analysis. Three biological replicate experiments were used to compare the proteomes of healthy control rats, a rat model of MTrP, MTrP model rats following dry needling of MTrPs, and MTrP model rats following dry needling of non-MTrPs.

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Neuropathic pain is a kind of chronic pain because of dysfunctions of somatosensory nerve system. Recently, many studies have demonstrated that microRNAs (miRs) play crucial roles in neuropathic pain development. This study was designed to investigate the effects of miR-134-5p on the process of neuropathic pain progression in a rat model established by chronic sciatic nerve injury (CCI).

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Objective: To examine the association between serum β2-microglobulin (B2M) levels and frailty in an elderly Chinese population.

Design: A population-based cohort study.

Setting And Participants: We used data on 1,663 elderly participants (aged 70-84 years) from the aging arm of the Rugao Longevity and Ageing study, a population-based observational two-arm cohort study conducted in Rugao, China.

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MicroRNAs (miRNAs) are reported as vital participators in the pathophysiological course of neuropathic pain. However, the underlying mechanisms of the functional roles of miRNAs in neuropathic pain are largely unknown. This study was designed to explore the potential role of miR-150 in regulating the process of neuropathic pain in a rat model established by chronic sciatic nerve injury (CCI).

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Neuropathic pain (NP) is a substantial clinical problem causing great injury to people word-widely. Although gene expression analyses had been performed previously, the mechanisms underlying the etiology and development of NP are still poorly understood. To understand the function genes involved in the etiology and development of NP, we built the co-expression modules and performed function enrichment analysis for neuropathic pain.

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Emerging evidence suggests that microRNAs (miRNAs) play a critical role in the pathogenesis of neuropathic pain. However, the exact role of miRNAs in regulating neuropathic pain remains largely unknown. In this study, we aimed to investigate the potential role of miR-93 in a rat model of neuropathic pain induced by chronic constriction sciatic nerve injury (CCI).

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Background/aims: Hypoxia has recently been proposed as one of the most important factors in progressive renal injury. Hypoxia-induced vascular endothelial growth factor (VEGF) expression may play a critical role in maintaining peritubular capillary endothelium in renal disease. This study was designed to investigate the effect and underlying mechanism of all-trans retinoic acid (ATRA) on hypoxia-induced injury in NRK52E cells.

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CRISPR-Cas9 (clustered regularly interspaced short palindromic repeats-CRISPR associated nuclease 9) systems have emerged as versatile and convenient (epi)genome editing tools and have become an important player in medical genetic research. CRISPR-Cas9 and its variants such as catalytically inactivated Cas9 (dead Cas9, dCas9) and scaffold-incorporating single guide sgRNA (scRNA) have been applied in various genomic screen studies. CRISPR screens enable high-throughput interrogation of gene functions in health and diseases.

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This is a retrospective study on the safety and efficacy of gamma knife radiosurgery (GKR) in treating hepatocellular carcinoma (HCC) with portal vein tumor thrombosis (PVTT). Patients with confirmed HCC and PVTT were allocated into two groups based on the treatments they received (palliative or GKR). A total of 138 patients were included (74 in the palliative group, 64 in GKR group).

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Article Synopsis
  • - Deletion of tumor suppressor genes, or oncosuppressors, is common in cancer genomes, but efforts to restore their function clinically have seen limited success.
  • - Alternative therapeutic strategies like "synthetic lethality" and "therapeutic vulnerability" can be utilized, as shown in a study by Liu et al, where the loss of both p53 and POLR2A in colon cancer cells made them especially sensitive to POLR2A inhibition.
  • - The article aims to explore various anticancer opportunities arising from oncosuppressor loss and highlights the need for further research in this area to improve cancer treatment.
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CRISPR-Cas9 is an RNA-guided site-specific DNA editing tool which, together with its reprogrammed versions such as nickase Cas9 and dead Cas9, enables quick modeling of desired combinations of cancer-associated genomic and/or epigenetic aberrations simultaneously or sequentially, thus facilitating massive functional interrogations and therapy testing.

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First introduced into mammalian organisms in 2013, the RNA-guided genome editing tool CRISPR-Cas9 (clustered regularly interspaced short palindromic repeats/CRISPR-associated nuclease 9) offers several advantages over conventional ones, such as simple-to-design, easy-to-use and multiplexing (capable of editing multiple genes simultaneously). Consequently, it has become a cost-effective and convenient tool for various genome editing purposes including gene therapy studies. In cell lines or animal models, CRISPR-Cas9 can be applied for therapeutic purposes in several ways.

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Objective: Leukemia cells can acquire a multidrug resistant (MDR) phenotype in response to a wide variety of chemotherapeutic agents including doxorubicin (Dox). In addition to the constitutive expression in the leukemia prior to chemotherapy, a complex phenotype of pleiotropic resistance is presented in the residual or recurrent leukemia. Recent studies showed Dox-induced coexpression of COX2 and MDR1 genes in human leukaemia cells, and whether Dox-induced MDR1 up-regulation in acute leukaemia cells is dependent on COX2-transcriptional activity and thus might be overcome or prevented with COX2-promotor inhibitor quercetin interfering with COX2 expression and activity.

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Competing endogenous RNAs (ceRNAs) refer to RNA transcripts, such as mRNAs, non-coding RNAs, pseudogene transcripts, and circular RNAs, that can regulate each other by competing for the same pool of miRNAs. ceRNAs involve in the pathogenesis of several common cancers such as prostate cancer, liver cancer, breast cancer, lung cancer, gastric cancer, endometrial cancer, and so on. ceRNA activity is determined by factors such as miRNA/ceRNA abundance, ceRNAs binding affinity to miRNAs, RNA editing, and RNA-binding proteins.

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The efficacy of combined vascular endothelial growth factor (VEGF) and epidermal growth factor receptor (EGFR) inhibition in patients with advanced non-small-cell lung cancer (NSCLC) was well studied. However, few studies focused on the risk and adverse events (AEs) of combined targeted therapy. The aim of this meta-analysis was to evaluate the safety profile of combined targeted therapy against EFGR and VEGF in patients with advanced NSCLC.

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Pseudogenes were initially regarded as non-functional genomic fossils resulted from inactivating gene mutations during evolution. However, later studies revealed that they play a plethora of roles at multiple levels (DNA, RNA and/or protein) in diverse physiological and pathological processes, especially in cancer, both parental-gene-dependently and parental-gene-independently. Pseudogenes can interact with parental genes or other gene loci, leading to alteration in their sequences and/or transcriptional activities.

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Most cancers develop upon the accumulation of genetic alterations that provoke and sustain the transformed phenotype. Several metabolomic approaches now allow for the global assessment of intermediate metabolites, generating profound insights into the metabolic rewiring associated with malignant transformation. The metabolomic profiling of neoplastic lesions growing in mice, irrespective of their origin, can provide invaluable information on the mechanisms underlying oncogenesis, tumor progression, and response to therapy.

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Background: A prospective randomized controlled trial was designed to observe the effect of tramadol on T-lymphocyte subsets, activated T cell and natural killer (NK) cells of patients undergoing gastric cancer surgeries.

Subjects And Methods: Thirty patients undergoing elective gastric cancer surgeries under general anesthesia were randomly divided into two groups. Before anesthesia induction, Group I did not receive any drugs and Group II received intramuscular tramadol 1 mg/kg.

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