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Soil hydraulic parameters are vital for precisely characterizing soil hydrological processes, which are critical indicators for regulating climate change effects on terrestrial ecosystems and governing feedbacks between water, energy, and carbon–nitrogen cycles. Although many studies have integrated comprehensive soil datasets, data quality and cost challenges result in data completeness deficiencies, especially for deep soil information. These gaps not only impede methodological endeavours but also constrain soil parameter-based ecosystem process studies spanning from local profiles to global earth system models. We established a soil dataset across the entire Yellow River Basin (YRB) (795,000 km2) using high-density in situ field sampling. This observation-based dataset contains records of soil texture (2924), bulk density (2798), saturated hydraulic conductivity (2782), and water retention curve parameters (1035) down to a maximum depth of 5 m. This dataset, which extends the recorded data range for deep soil hydraulic parameters, is valuable as a direct data resource for environmental, agronomical and hydrological studies in the YRB and regions with similar pedological and geological backgrounds around the world. [ABSTRACT FROM AUTHOR]

Objective: Glucose-dependent insulinotropic polypeptide (GIP) is an incretin hormone which has been ascribed a positive role in cardiovascular function. However, little is known about the association between GIP and microvascular complications including retina and kidney. In the present study, we conducted a cross-sectional study to investigate the relationship between fasting serum GIP and microvascular complications in type 2 diabetes mellitus (T2DM). Methods: A cross-sectional study was performed in 295 T2DM patients in our endocrine ward in order to investigate the relationship between fasting serum GIP and microvascular complications. Results: Among the 295 T2DM patients, the levels of median fasting serum GIP of all were 431.36pg/ml, interquartile range of which were 333.26~531.96pg/ml and the prevalence of diabetic retinopathy (DR) and diabetic nephropathy (DN) were 37.63% and 38.64% respectively. Our study observed that the prevalence of DR was significantly higher in low-levels GIP group compared with those in high-levels GIP group (p=0.007) (46.26% versus 31.08%) and the levels of fasting serum GIP were also higher in T2DM patients without DR than those with DR (p=0.019) (440.99pg/ml versus 405.90pg/ml). Spearman's correlation and multiple stepwise regression analysis showed that prevalence of DR was independently and negatively correlated with fasting serum GIP in T2DM (r=−0.134, p=0.021) (DR,β= −0.279; 95% CI, −0.512~−0.047, p = 0.019). However, there were no differences in fasting serum GIP between non-proliferative diabetic retinopathy (NPDR) and proliferative diabetic retinopathy (PDR) (p=0.951). Similarly, we did not find any association between fasting serum GIP and prevalence of DN by using various statistical analyses. Conclusions: Prevalence of DR was independently and negatively correlated with fasting serum GIP in T2DM, indicating that elevated levels of fasting serum GIP may act as protective factors for DR. [ABSTRACT FROM AUTHOR]

Iodine is an important chemical for thyroid hormone synthesis. The association between iodine nutrition status and the risk of disease present U-shaped curve, as either low or high iodine nutrition status will increase the risk of thyroid diseases. Endoplasmic reticulum stress (ER stress), which can induce over expressions of inflammation factors, like monocyte chemo-attractant protein-1 (MCP-1), is related to the pathogenesis of thyroid disease. However, the correlations among iodine, MCP-1 and ER stress are not entirely clear during the pathogenesis of thyroid diseases. Present study aims to investigate how iodine nutrition status influences MCP-1 expression through P38/MAPK pathway as well as the roles of ER stress in this process. Human thyroid cells (Nthy-ori-3-1) was used as a cell model in this study. The expressions of p-P38, PERK, IRE1, ATF6, and MCP-1 were detected after the cells were treated with iodine at different concentrations with or without ER stress inhibitor (4-PBA) or P38/MAPK blocker (SB203580). The expressions of p-P38, PERK, IRE1, ATF6, and MCP-1 in Nthy-ori-3-1 cells treated with iodine at abnormal concentrations were all significantly higher than those in cells treated with iodine at normal concentration. However, addition of ER stress blocker, 4-PBA in the abnormal-iodine treated cells, decreased the expressions of p-P38, PERK, IRE1, ATF6, and MCP-1. Similarly, P38/MAPK activity inhibitor, SB203580, also decreased the expressions of p-P38 and MCP-1. Abnormal iodine nutrition status triggered ER stress and upregulated MCP-1 expression through P38/MAPK signaling pathway in thyrocyte. [ABSTRACT FROM AUTHOR]