Health risk assessment and potential sources of metals in riparian soils of the Wujiang River, China.

In order to understand the pollution status of metals in the riparian soils along the Wujiang River, 26 sampling sites in the mainstream and tributary streams were selected for investigation. The geo-accumulation index (Igeo), Nemerow integrated pollution index, and potential ecological risk index were applied to evaluate the contamination status and ecological risks of metals. Results revealed that the average concentrations of As, Cd, Cr, Cu, Mn, Ni, Pb, and Zn were 12.20, 0.51, 84.01, 57.42, 922.57, 38.37, 38.06, and 127.82 mg/kg, respectively. The metal contamination degree and ecological risks in the upper reaches were significantly higher than those in the middle and lower reaches of the Wujiang River. Cd was the dominant contamination metal. Significant non-carcinogenic and carcinogenic risks of metals were found in children based on the hazard index and carcinogenic risk. As was the main non-carcinogenic and carcinogenic pollutant metal in both adults and children. According to principal component analysis, hierarchical clustering analysis, and absolute principal component scores-multiple linear regression, anthropogenic sources (mining and agricultural activities) contributed most to Zn, Pb, Cr, Cd, Cu, and Ni, with contribution rates of 89.14, 82.32, 74.46, 72.12, 68.52, and 61.02%, respectively. Natural sources contributed most to Mn, with a contribution rate of 83.07%. Unidentified sources contributed most to As, with a contribution rate of 47.27%.

Novel serum biomarker of Golgi protein 73 for the diagnosis of clinically significant portal hypertension in patients with compensated cirrhosis.

Hepatic venous pressure gradient (HVPG) is the gold standard for evaluating clinically significant portal hypertension (CSPH). However, reliable noninvasive methods are limited. Our study aims to investigate the diagnostic value of serum Golgi protein 73 (GP73) for CSPH in patients with compensated cirrhosis. The study enrolled 262 consecutive patients with compensated cirrhosis from three centers in China from February 2021 to September 2023, who underwent both serum GP73 tests and HVPG measurements. CSPH was defined as HVPG ≥ 10 mmHg. Diagnostic accuracy was evaluated using the areas under the receiver operating characteristic curve (AUC). The prevalence of CSPH was 56.9% (n = 149). There were significant differences between the CSPH and non-CSPH groups in the median serum GP73 level (126.8 vs. 73.1 ng/mL, p < 0.001). GP73 level showed a significant positive linear correlation with HVPG (r = 0.459, p < 0.001). The AUC for the diagnosis of CSPH using serum GP73 alone was 0.75 (95% confidence interval [CI] 0.68-0.81). Multivariate logistic regression analysis determined that the levels of GP73, platelets and international normalized ratio were independently associated with CSPH. The combination of these three markers was termed "IP73" score with an AUC value of 0.85 (95% CI 0.80-0.89) for CSPH. Using 0 as a cut-off value, the specificity and sensitivity of IP73 score were 77.9% and 81.9%, respectively. The IP73 score offers a novel, simple and noninvasive method of assessing CSPH in patients with compensated cirrhosis. A cut-off value of the IP73 score at 0 can distinguish patients with or without CSPH.

Role of Hydrogen Sulfide and Hypoxia in Hepatic Angiogenesis of Portal Hypertension.

The pathogenesis of portal hypertension remains unclear, and is believed to involve dysfunction of liver sinusoidal endothelial cells (LSEC), activation of hepatic stellate cells (HSC), dysregulation of endogenous hydrogen sulfide (H2S) synthesis, and hypoxia-induced angiogenic responses. H2S, a novel gas transmitter, plays an important role in various pathophysiological processes, especially in hepatic angiogenesis. Inhibition of endogenous H2S synthase by pharmaceutical agents or gene silencing may enhance the angiogenic response of endothelial cells. Hypoxia-inducible factor-1 (HIF-1) is the main transcription factor of hypoxia, which induces hepatic angiogenesis through up-regulation of vascular endothelial growth factor (VEGF) in HSC and LSEC. H2S has also been shown to be involved in the regulation of VEGF-mediated angiogenesis. Therefore, H2S and HIF-1 may be potential therapeutic targets for portal hypertension. The effects of H2S donors or prodrugs on the hemodynamics of portal hypertension and the mechanism of H2S-induced angiogenesis are promising areas for future research.