Publications by authors named "Danli Cai"

Article Synopsis
  • - Studies indicate a strong link between the microbiota and gastric cancer (GC), showing that patients with GC have significantly different gastric microbiota compared to non-cancer patients, which suggests that these microbes may contribute to GC development.
  • - While certain infections, like () infection, are well-known risk factors for GC, recent research highlights that non-microbes also play a crucial role in the disease's progression and can lead to precancerous lesions.
  • - Novel diagnostic technologies, such as PCR and genetic testing, are being used to identify microbial markers associated with precancerous lesions in the stomach, aiming to uncover new strategies for the prevention and treatment of these lesions.
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Article Synopsis
  • The study focuses on improving the diagnosis of Precancerous Lesions of Gastric Cancer (PLGC) by analyzing chromosome copy number variations (CNV) using data from the TCGA database and UCAD techniques.
  • CNV analysis revealed significant amplifications on chromosomes 7, 8, and 17 in gastric cancer patients, while UCAD confirmed a positive Chromosomal Instability (CIN) detection rate of 41.7% in severe atrophy cases.
  • The results indicate that UCAD's CIN measurements, particularly those related to chromosomes 7 and 8, could enhance the diagnostic process for PLGC, proving more sensitive than traditional tumor indicators.
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Gastric cancer (GC) is a prevalent malignant tumor within the digestive system, with over 40% of new cases and deaths related to GC globally occurring in China. Despite advancements in treatment modalities, such as surgery supplemented by adjuvant radiotherapy or chemotherapeutic agents, the prognosis for GC remains poor. New targeted therapies and immunotherapies are currently under investigation, but no significant breakthroughs have been achieved.

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Objective: To evaluate the protective efficacy of Sanqi (Radix Notoginseng) on cerebral hemorrhage in a rat model of traumatic brain injury (TBI) by investigating plasminogen activator inhibitor-1 (PAI-1), tissue-type plasminogen activator (t-PA), nuclear factor-κB (NF-κB, p-p65), nitric oxide (NO), endothelin (ET), cluster differentiation (CD61CD62), and coagulation.

Methods: The free-fall method was used to create a rat model of TBI. Forty-eight rats were randomly divided into six groups: the blank group, sham group, model group, low-dose Sanqi (Radix Notoginseng) group, middle-dose Sanqi (Radix Notoginseng) group, and high-dose Sanqi (Radix Notoginseng) group.

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Objective: To verify the feasibility of treating pressure ulcers (PUs) with autologous platelet-rich fibrin-based (PRF) bioactive membrane, both in vitro and in vivo.

Method: An animal model using adult male Sprague-Dawley rats was used. Pressure was periodically exerted on the skin to induce localised ischaemia by using an external magnet and transplanted metal disc.

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Inflammatory response is an important determining factor for the mortality of patients with pulmonary thromboembolism. Inflammatory mediators can promote thrombus formation and increase hemodynamic instability. Urokinase is a commonly used drug for the treatment of PTE.

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Objective: To explore the changes of Sonic Hedgehog (Shh) signaling pathway in the stomach mucosa during the formation of gastric precancerous lesions.

Methods: A total of 72 suckling rats in half genders were randomly and equally divided into the normal group and model group. The rats in the model group were administered with 0.

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Objective: To observe the effect of electroacupuncture (EA) at ST36 on the intestinal mucosal mechanical barrier and expression of the tight junction (TJ) protein, occludin, in a rat model of sepsis.

Methods: 60 male Wistar rats were randomly divided into six groups (n=10 rats each): Control, Control+EA, CLP (caecal ligation and puncture), CLP+EA, CLP+Sham-EA, and Sham-CLP. Rats of the CLP, CLP+EA and CLP+Sham-EA groups underwent CLP modeling of sepsis; those in the Sham-CLP underwent sham surgery and those in the Control and Control+EA groups remained unoperated.

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The purpose of the present study was to examine whether aspirin interferes with the inflammatory response in a thrombus‑stimulated lung microvascular endothelial cell (LMVEC) model. The LMVECs were randomly divided into eight groups: Normal group (group N), model group (group M), model + ASP group (group M+A), model+CX3CL1‑short hairpin (sh)RNA group (group M+SH), model + CX3CL1‑overexpression vector group (group M+CX3), model + ASP + shRNA group (group M+A+SH), model + ASP + CX3CL1‑overexpression vector group (group M+A+CX3), and normal + virus control group (group N+V). The endothelial cells were cultured, and a thrombus was added to the cells.

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The present study aimed to explore the influence of aspirin on the CX3CL1/CX3CR1 signaling pathway in acute pulmonary embolism (APE) in rats. Our previous study found that CX3CL1/CX3CR1 was increased in APE. However, the effect of this signaling pathway on APE remains unclear.

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