Publications by authors named "Na-Juan Cui"

Background: The drug instructions for dabigatran recommend adjusting the dosage to 110 mg twice daily for patients with bleeding risk, and performing at least one renal function test per year for patients with moderate renal impairment. However, owing to chronic insidiously worsening renal insufficiency, dabigatran can still accumulate abnormally, necessitating therapy with idarucizumab to reverse the anticoagulation due to severe erosive gastritis with widespread stomach mucosal bleeding.

Case Summary: A 76-year-old woman with a history of atrial fibrillation who took dabigatran 110 mg twice daily as directed to lessen the chance of stroke, was transported to the hospital with hematemesis and melena.

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Objective: To explore the relationship between the genesis of Pi-Wei damp-heat syndrome (PDS) and the Helicobacter pylori (HP) infection in patients with chronic gastritis (CG) by observing the levels of nuclear factor kappaB (NF-kappaB) mRNA and heat shock protein 70 (HSP70) expressions.

Methods: Gastric mucous membrane tissues collected through gastroscopy from gastric antrum of 51 CG patients, 36 of PDS type (CG-PDS) and 15 of Pi-qi deficiency syndrome (CG-non-PDS) type, and 8 healthy persons (as control) were examined to diagnose the inflammation level with HE stain and to detect the existence of HP infection by rapid urease test and methylthioninium chloride stain. The mRNA expressions of NF-kappaB and HSP70 in the tissues were determined quantitatively with FQ-PCR as well.

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It has been proved in recent studies that the chronic gastric disease (CGD) of Pi-Wei damp-heat syndrome type (CGD-PWDH) is closely related with heat shock protein 70 (HSP70) and nuclear factor-kappa B (NF-kappaB). HSP70 can protect the auto-stability of cells and elevate the immune function in organism against tumor or multiple exogenous pathogens. Increasing of NF-kappaB expression presents in case of Helicobacter pylori (Hp) stimulation, it could induce inflammatory reaction, while inflammation factors could act inversely to enhance the expression of NF-kappaB, thus to cause and expand the damage of gastric mucosa.

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