Publications by authors named "Ji-Zheng Guo"

The matrix glycoprotein thrombospondin-1 (THBS1) modulates nitric oxide (NO) signaling in endothelial cells. A high-salt diet induces deficiencies of NO production and bioavailability, thereby leading to endothelial dysfunction. In this study we investigated the changes of THBS1 expression and its pathological role in the dysfunction of mesenteric artery endothelial cells (MAECs) induced by a high-salt diet.

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Cardiovascular diseases are related to vascular endothelial cell injury; our previous studies showed that endosulfan could cause hypercoagulation of blood by inducing endothelial cell injury. To clarify the mechanism of it, we treated human umbilical vein endothelial cells (HUVECs) with 0, 1, 5, and 10 μg/mL endosulfan, while in the inhibition groups, reactive oxygen species (ROS) inhibitor N-acetylcysteine (NAC, 3 mmol) and endoplasmic reticulum (ER) stress inhibitor (STF-083010, 10 μmol) were incubated prior to endosulfan. The results showed that endosulfan could induce inflammatory response and dysfunction by increasing the release of inflammatory cytokines such as interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), and adhesion molecules such as vascular cell adhesion molecule 1 (VCAM-1) and endothelin-1 (ET-1), and inducing ROS production in HUVECs.

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It is well known that high-risk human papilloma virus (HR-HPV) infection is strongly associated with cervical cancer and E7 was identified as one of the key initiators in HPV-mediated carcinogenesis. Here we show that lactate dehydrogenase A (LDHA) preferably locates in the nucleus in HPV16-positive cervical tumors due to E7-induced intracellular reactive oxygen species (ROS) accumulation. Surprisingly, nuclear LDHA gains a non-canonical enzyme activity to produce α-hydroxybutyrate and triggers DOT1L (disruptor of telomeric silencing 1-like)-mediated histone H3K79 hypermethylation, resulting in the activation of antioxidant responses and Wnt signaling pathway.

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Introduction: mTOR and MDM2 signaling pathways are frequently deregulated in cancer development, and inhibition of mTOR or MDM2 independently enhances carcinoma-cell apoptosis. However, responses to mTOR and MDM2 antagonists in renal cell carcinoma (RCC) remain unknown.

Materials And Methods: A498 cells treated with MDM2 antagonist MI-319 and/or mTOR inhibitor rapamycin were employed in the present study.

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Article Synopsis
  • A study aimed to assess how the disruption of the internal iliac artery impacts blood flow and erectile function in patients who underwent renal transplantation.
  • The research involved 33 chronic renal failure patients, measuring erectile function and penile blood flow before and after their transplant.
  • Findings indicated that while blood flow decreased post-surgery, it did not significantly affect erectile function, with many patients reporting unchanged or improved sexual desire following their transplant.
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Objective: To summarize the clinical experience in living related donor kidney transplantation.

Methods: 117 patients with different nephropathies underwent transplantation of kidneys donated by their collateral relative in three generations. All donor kidneys were removed by open nephrectomy.

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Article Synopsis
  • A study of 824 male renal transplant recipients found that a high prevalence of erectile dysfunction (ED) exists, with 75.5% reporting some level of ED, categorized into mild, moderate, and severe cases.
  • The prevalence of ED increases with age, with rates reaching 92.2% in patients over 60 years, alongside a corresponding rise in the severity of ED in older groups.
  • Factors such as occupation and education level also influenced ED rates, revealing that those without employment and with lower educational attainment experienced higher instances of erectile dysfunction.
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The quality of sexual life is important for renal transplantation recipients. With the increase of survival rate of renal transplantation, the quality of the male recipients' sexual life, especially their erectile function, has been generally remarked. The prevalence of ED is 35.

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Objective: To study the role of baseline risk factors in predicting the onset of diabetes among essential hypertensive patients with metabolic syndrome (MS) and to evaluate an ideal therapeutic regime that could reduce the risk factors and risk of onset of diabetes.

Methods: A randomized parallel clinical trial in essential hypertensive patients of grade 1 or 2 was conducted. Two of the three components (1) increased waist circumference and/or BMI; (2) increased triglycerides (TG) and/or decreased high-density lipoprotein cholesterol; (3) impaired glucose tolerance (IGT) were present define the MS.

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