Publications by authors named "Yingjing Shen"

Background: The bone-vascular axis plays a key role in the pathogenesis of vascular calcification (VC) in patients with chronic kidney disease (CKD). Understanding and managing the role of the bone-vascular axis in CKD-mineral and bone disorder (CKD-MBD) is critical for preventing and treating associated complications, including osteoporosis, arterial calcification, and cardiovascular diseases. This study aimed to comprehensively summarize the role of bone metabolism markers in uremic VC.

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In extracorporeal circulation, inflammatory mediators are eliminated through inflammatory cytokine adsorption. By interacting with inflammatory cytokines and removing them from the bloodstream, the adsorber's adsorbent lowers levels of inflammatory mediators and the inflammatory response. We present the case of a 67-year-old Chinese man diagnosed with sepsis due to a bloodstream infection from a catheter.

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This review elucidates the modeling and mechanistic studies of vascular calcification in chronic kidney disease - mineral and bone disorder. In patients with chronic kidney disease, metabolic abnormalities in uremic toxins, including phosphate and indole sulfate, are closely associated with vascular calcification. Vitamin K, vascular circadian clock, and autophagy are also key factors involved in vascular calcification.

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Chronic kidney disease-mineral and bone disorder is a syndrome of mineral and bone metabolism abnormalities caused by chronic kidney disease. Osteoporosis is a systemic metabolic bone disease characterized by low bone mass, disruption of bone microstructure, increased brittleness, and a higher propensity for fractures. Both of these conditions significantly affect bone metabolism and substantially increase the risk of fractures.

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Chronic kidney disease-mineral and bone disorder has complex and diverse clinical manifestations, including the simplest abnormalities of calcium, phosphorus and parathyroid hormone detected in blood, abnormalities of bone transformation and mineralization in bone, and calcification of blood vessels or other soft tissues detected on imaging. Patients with CKD-MBD combined low bone mineral density and fragility fractures are referred to as CKD-MBD with low bone mineral density. Vascular calcification refers to ectopic deposition of calcium phosphate in the blood vessel walls and heart valves.

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Background: Hypercalcemia crisis is a complex disorder rarely induced by tertiary hyperparathyroidism, which clinically presents as nonsuppressible parathyroid hyperplasia with persistent increased PTH levels and hypercalcemia. It is one of the major risk factors of morbidity and mortality in end-stage renal disease. Parathyroidectomy should be in consideration in dialysis patients with severe hyperparathyroidism who are refractory to medical therapy.

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Introduction: This report describes the novel sampling of autosomal dominant polycystic kidney disease (ADPKD) combined with hypertrophic cardiomyopathy (HCM).

Symptoms And Clinical Findings: A 48-year-old Chinese man presented with anasarca, hypourocrinia, gross hematuria, and weight gain by 10 kg subsequently developed acute kidney injury after struck by acute respiratory distress syndrome, really a threat to his heart.

Diagnoses: Abdominal ultrasound revealed multiple small cysts in both kidneys, with the right kidney measuring 11.

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Although it has been suggested that REL is the critical target gene of 2p12-16 amplification in diffuse large B-cell lymphoma (DLBCL), little experimental evidence supports this notion. In the present study, we sought to evaluate the relationship between REL amplification and REL function in a panel of 46 newly diagnosed DLBCLs and to correlate with DLBCL subgroups as identified by gene expression profiles and clinical features. The results indicate that amplification of the REL locus is not associated with accumulation of the active form of REL, as evaluated by immunofluorescence analysis.

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