Relationship between serum phosphorus and mortality in non-dialysis chronic kidney disease patients: evidence from NHANES 2001-2018.

BACKGROUND: Hyperphosphatemia is common in chronic kidney disease (CKD), associated with higher mortality in dialysis patients. Its impact in non-dialysis patients, especially those with preserved kidney function, remains uncertain. METHODS: A prospective cohort study was conducted using data from the National Health and Nutrition Examination Survey (2001-2008). Serum phosphorus was analyzed as a continuous variable, or categorized into three groups: < 3.5 mg/dL, 3.5 to < 4.5 mg/dL, and ≥ 4.5 mg/dL. Cox proportional hazards models were used to analyze the association between phosphorus with all-cause and cardiovascular disease (CVD) mortality, with or without adjustment for age, sex, race, hemoglobin, estimated glomerular filtration rate (eGFR), serum albumin, serum calcium, 25(OH)D, obesity, hypertension, diabetes, and CVD. RESULTS: A total of 7694 participants were included in the analysis, representing 28 million CKD patients in the United States. During mean 92 months of follow up, 2708 all-cause deaths (including 969 CVD deaths) were observed. Per 1 mg/dL increase in phosphorus was associated with a 13% and 24% increased risk of all-cause mortality (hazard ratio [HR], 1.13; 95%CI, 1.02-1.24) and CVD mortality (HR, 1.24; 95%CI, 1.07-1.45), respectively. Compared with the < 3.5 mg/dL, phosphorus ≥ 4.5 mg/dL was associated with a 28% and 57% increased risk of all-cause mortality (HR, 1.28; 95%CI, 1.05-1.55) and CVD mortality (HR, 1.57; 95CI, 1.19-2.08), respectively. In participants with eGFR < 60 ml/min/1.73m2, elevated phosphorus (≥ 4.5 mg/ dL) were significantly associated with increased risk of all-cause mortality (HR, 1.36; 95%CI, 1.07-1.72). No significant association was observed in eGFR ≥ 60 ml/min/1.73m2 group (HR, 1.31; 95%CI, 0.86-1.99). This correlation does not differ significantly between subgroups defined by eGFR level (P for interaction = 0.889). CONCLUSION: Serum phosphorus above 4.5 mg/dL is significantly associated with a 28% and 57% increased risk of all-cause and CVD death in non-dialysis CKD patients, respectively. This relationship still demonstrated in patients with eGFR < 60 ml/min/1.73m2. However, for population with eGFR ≥ 60 ml/min/1.73m2, further verification is needed.

Nano­selenium alleviates the pyroptosis of cardiovascular endothelial cells in chicken induced by decabromodiphenyl ether through ERS-TXNIP-NLRP3 pathway.

Decabromodiphenyl ether (BDE-209) is one of the most widely used flame retardants that can infect domestic and wildlife through contaminated feed. Nano­selenium (Nano-Se) has the advantage of enhancing the anti-oxidation of cells. Nonetheless, it remains uncertain whether Nano-Se can alleviate vascular Endothelial cells damage caused by BDE-209 exposure in chickens. Therefore, we established a model with 60 1-day-old chickens, and administered BDE-209 intragastric at a ratio of 400 mg/kg bw/d, and mixed Nano-Se intervention at a ratio of 1 mg/kg in the feed. The results showed that BDE-209 could induce histopathological and ultrastructural changes. Additionally, exposure to BDE-209 led to cardiovascular endoplasmic reticulum stress (ERS), oxidative stress and thioredoxin-interacting protein (TXNIP)-pyrin domain-containing protein 3 (NLRP3) pathway activation, ultimately resulting in pyroptosis. Using the ERS inhibitor 4-PBA in Chicken arterial endothelial cells (PAECs) can significantly reverse these changes. The addition of Nano-Se can enhance the body's antioxidant capacity, inhibit the activation of NLRP3 inflammasome, and reduce cellular pyroptosis. These results suggest that Nano-Se can alleviate the pyroptosis of cardiovascular endothelial cells induced by BDE-209 through ERS-TXNIP-NLRP3 pathway. This study provides new insights into the toxicity of BDE-209 in the cardiovascular system and the therapeutic effects of Nano-Se.

Adsorption mechanism of phosphorus on biomass ash modified with lanthanum immobilized by chitosan.

The immobilized lanthanum-modified biomass ash gel ball (CS-La-BA) was prepared with lanthanum chloride, biomass ash, and chitosan to remove phosphorus from water. CS-La-BA was characterized by several analytical techniques. SEM-EDS results showed that CS-La-BA has a well-developed pore structure and abundant adsorption sites. The surface area of BET is 75.46 m2/g and the pore size is mostly at 1.84 nm, indicating that it is a composite porous material with abundant microporous structure. The presence of La on biomass ash and the charge property of CS-La-BA were determined by XRD and zeta potential, and the adsorption mechanism of CS-La-BA on phosphate, including precipitation, electrostatic adsorption, ligand exchange, and complexation mechanism, was revealed by FTIR and XPS. The effects of pH, temperature, adsorbent dosage, initial phosphorus concentration, adsorption time, and coexisting ions on the phosphorus uptake performance of CS-La-BA were discussed. The adsorption experiment results show that the phosphorus removal rate of CS-La-BA can reach 95.6%. Even after six desorption and regeneration experiments, the phosphorus removal rate still reaches 68.13%, which indicates that CS-La-BA has good phosphorus adsorption performance and desorption and regeneration capacity. The phosphorus adsorption process of CS-La-BA conforms to the Freundlich isotherm adsorption equation and general-order kinetic model. The internal diffusion of the adsorption process is dominant, and the maximum adsorption capacity is 31.73 mg/g (25 ℃). Thermodynamic experiments show that the adsorption process of phosphorus by CS-La-BA is a spontaneous entropy increase process.

Atheroprotective Effects and Mechanisms of Postmarketing Chinese Patent Formulas in Atherosclerosis Models: A Systematic Review.

BACKGROUND: Some postmarketing Chinese patent formulas have been widely used to treat atherosclerosis (AS) and play critical roles in Chinese healthcare. However, the usage of these herbs is yet controversial due to unclear effects and lack of understanding of the mechanism of action. With the modernization of traditional Chinese formulas, we are to elucidate the atheroprotective properties of these remedies from successful postmarketing experiments in vivo. METHODS: In this systematic review, we critically searched the databases, applied stringent criteria, assessed the methodological quality, and examined the current evidence in vivo. RESULTS: Consequently, 60 studies were included in the present qualitative synthesis. Data on models, high-fat diet, intervention time, outcome measures, efficacy, and mechanisms were collected. Finally, 23 formulas that could alleviate AS were correlated to the amelioration of plaques, improvement of plaque stability, modification of lipid level and lipid metabolism, and the effects of anti-inflammation and antioxidant stress with multiple components and targets. However, the methodological quality was low and incomplete among the included literature. CONCLUSIONS: Thus, taken together, the studies on postmarketing Chinese patent formulas would provide a novel approach to improve the treatment of AS, and rigorously designed studies would provide high-quality evidence.

Qiliqiangxin Capsules Optimize Cardiac Metabolism Flexibility in Rats With Heart Failure After Myocardial Infarction.

Metabolic modulation is a promising therapy for ischemic heart disease and heart failure. This study aimed to clarify the regional modulatory effect of Qiliqiangxin capsules (QLQX), a traditional Chinese medicine, on cardiac metabolic phenotypes. Sprague-Dawley rats underwent left anterior descending coronary artery ligation and were treated with QLQX and enalapril. Striking global left ventricular dysfunction and left ventricular remodeling were significantly improved by QLQX. In addition to the posterior wall, QLQX also had a unique beneficial effect on the anterior wall subject to a severe oxygen deficit. Cardiac tissues in the border and remote areas were separated for detection. QLQX enhanced the cardiac 18F-fluorodeoxyglucose uptake and the levels and translocation of glucose transport 4 (GLUT4) in the border area. Meanwhile, it also suppressed glucose transport 1 (GLUT1) in both areas, indicating that QLQX encouraged border myocytes to use more glucose in a GLUT4-dependent manner. It was inferred that QLQX promoted a shift from glucose oxidation to anaerobic glycolysis in the border area by the augmentation of phosphorylated pyruvate dehydrogenase, pyruvate dehydrogenase kinases 4, and lactic dehydrogenase A. QLQX also upregulated the protein expression of fatty acid translocase and carnitine palmitoyl transferase-1 in the remote area to possibly normalize fatty acid (FA) uptake and oxidation similar to that in healthy hearts. QLQX protected global viable cardiomyocytes and promoted metabolic flexibility by modulating metabolic proteins regionally, indicating its potential for driving the border myocardium into an anaerobic glycolytic pathway against hypoxia injuries and urging the remote myocardium to oxidize FA to maximize energy production.

Effect of orally administered hydroxypropyl chitosan on the levels of iron, copper, zinc and calcium in mice.

Two hydroxypropyl chitosan HPCS samples (HPCS1 Mw 1.6 × 10(5), HPCS2 Mw 3.5 × 10(4)) were prepared by the reaction of chitosan with propylene oxide under alkali conditions. The median lethal dose of the hydroxypropyl chitosan was greater than 10 g/kg for the laboratory mice. HPCS1 at the 0.1%, 1.0%, 1.5% and HPCS2 at the 1.0% level in diets were used to feed the mice for 90 days respectively. No pathological symptoms, clinical signs or deaths were observed for all mice. The weights of the mice in HPCS groups and control group had no significant difference. The levels of Fe, Cu, Zn and Ca in the mice were measured by atomic absorption spectrophotometry. HPCS had no significant effect on the levels of Fe, Cu, Zn and Ca in the tested mice's livers and hearts. However, hydroxypropyl chitosan at high dose exhibited inhibitory effects on the levels of Fe, Zn and Ca in some organizations.