Publications by authors named "Jing-Juan Ding"

Article Synopsis
  • Macrophages significantly influence vascular diseases, and their function is tied to changes in metabolism, particularly in the context of diabetes.
  • Researchers identified a circular RNA called cSPECC1 that increases in diabetic conditions and affects macrophage behavior, particularly in preventing inflammation and maintaining communication with endothelial cells.
  • By manipulating cSPECC1 levels, they found it plays a crucial role in macrophage function and could be a potential target for new treatments aimed at reducing vascular issues in diabetes.
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Background: Pathological neovascularization plays a pivotal role in the onset and progression of tumors and neovascular eye diseases. Despite notable advancements in the development of anti-angiogenic medications that target vascular endothelial growth factor (VEGF) and its receptors (VEGFRs), the occurrence of adverse reactions and drug resistance has somewhat impeded the widespread application of these drugs. Therefore, additional investigations are warranted to explore alternative therapeutic targets.

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Background: Ocular neovascularization is a leading cause of blindness and visual impairment. While intravitreal anti-VEGF agents can be effective, they do have several drawbacks, such as endophthalmitis and drug resistance. Additional studies are necessary to explore alternative therapeutic targets.

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Wet age-related macular degeneration (wAMD) is the leading cause of blindness among the elderly in industrialized nations. Anti-vascular epidermal growth factor (VEGF) therapy via intravitreal injection is the most effective clinical treatment for wAMD due to high concentrations of VEGF that promote choroidal neovascularization. While PIWI proteins participate in various biological processes, their function in AMD remains unclear.

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Objective: To investigate hepatitis B virus (HBV) subtypes in patients chronically infected with genotype B or C of hepatitis B virus in Guizhou and to study the relationship between the subtypes and the progression of their liver diseases.

Methods: Using PCR, 309 bp gene fragments in the HBV p region were amplified. The products of PCR were digested by VspI, NciI, BstEII and subjected to agarose gel electrophoresis.

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Objective: To investigate the distribution of hepatitis B virus (HBV) precore A1896 and basic core promoter (BCP)T1762/A1764 mutations in Guizhou area.

Methods: 482 patients with chronic HBV infection, belonging to 4 nationalities, including 225 asymptomatic carriers (ASC), 158 chronic hepatitis (CH), 57 liver cirrhosis (LC), 42 hepatocellular carcinoma (HCC), from 4 areas of Guizhou province were examined. HBV A1896 and T1762/A1764 mutations were determined by direct sequencing and restriction fragment length polymorphism (RFLP).

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Objective: To establish a mismatched polymerase chain reaction restricted fragment length polymorphism (mPCR-RFLP) method for detection of hepatitis B virus (HBV) mutation in precore A1896, and compare with direct sequencing for evaluating its applicability.

Methods: According to the principle of mPCR, 194bp gene fragments in HBV precore region was amplified. The products of PCR were digested by Bsu36I and subjected to agarose gel electrophoresis.

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Objective: To investigate the distribution of hepatitis B virus (HBV) genotype in Guizhou and to study the relationship between the genotype and the progression of liver disease.

Methods: 786 patients with chronic HBV infection, from 4 cities of Guizhou, including 346 asymptomatic carriers (ASC), 313 chronic hepatitis (CH), 77 liver cirrhosis (LC), 50 hepatocellular carcinoma (HCC) were examined. HBV genotype was determined by restriction fragment length polymorphism analysis and the subtypes were determined by direct sequencing of PCR product in 94 patients with HBV B genotype, the relationship between HBV genotype and the progression of liver disease was studied by multifactor analysis such as HBeAg positivity, HBV DNA load and ALT level.

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Objective: To study the relationships between hepatitis B virus (HBV ) pre-S region mutations and their genotypes and the stages of liver disease of the patients.

Methods: The entire HBV pre-S1 and pre-S2 genes were amplified by polymerase chain reaction (PCR). The amplified products were digested by NlaIII restriction enzyme.

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Objective: To study the distribution of hepatitis B virus (HBV) genotype in population of Dong, Miao minority and Han in Guizhou.

Methods: S region nucleotides were compared in 127 strains whole sequence of HBV and three restriction enzymes which can be used for genotyping were found by DNA software analysis system. The partial gene fragment of HBV S region was amplified by nested polymerase chain reaction (nPCR).

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Objective: To establish a simple and accurate method for rapid detection of lamivudine related mutations in hepatitis B virus (HBV) polymerase gene.

Methods: HBV polymerase gene fragments of covering B and C active region were amplified by nested polymerase chain reaction (nPCR) or nested mismatched PCR. The PCR products were digested with Nde I or Nia III and subjected to electrophoresis on agarose gel, respectively.

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Objective: To establish a new polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method of genotyping HBV using Mbo I, BsTN I, BsmA I, Hpa II and investigate the relationship between genotype and clinical spectrum of hepatitis B.

Methods: 124 full-genomic HBV sequences and 13 S-genomic sequences were analyzed, genotype specific regions were identified by the restriction enzymes Mbo I, BsTN I, BsmA I, Hpa II. And 176 samples from different kinds of hepatitis B were genotyped by this method.

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Background: To establish a new assay for detecting the quantity of HBV DNA with PCR and enzyme-linked immunosorbent assay(ELISA).

Methods: The products of PCR using primers pre-labeled with biotin were hybridized with the capture probes that were immobilized on the microtiter strips and then bond with Sav-Ap. The quantity of DNA was detected by measuring the yellow color at 405 nm wave length.

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