Source and sequestration of sediment organic carbon from different elevation zones in estuarine wetland, North China.

Estuarine wetland plays an important role in regulating global carbon cycle due to high terrestrial carbon input and burial. However, it is unclear how the source and sequestration of sediment organic carbon (SOC) in estuarine wetlands changes under the anthropogenic impact in the past century. In this study, combining parameters of TOC/TN ratios, δ13C, δ15N and 210Pb-chronology, temporal trends of SOC source and sequestration flux in Liaohe estuarine wetland were studied. The results showed that the source of organic carbon in Liaohe estuarine wetland was dominated by terrestrial input (contribution >60 %). Due to vegetation, TOC in shallow reed marsh was significantly higher than that of bare beach and subtidal flat. Affected by elevation, the sediment mass accumulation rate (MAR, kg·m-2·yr-1) showed differences in reed marsh (C1), bare beach (C2) and subtidal flat (C3), which were 6.57, 13.56 and 13.25 respectively in the past century. MAR fluctuated over time, it showed an overall increasing trend, especially since the 1980s. Correspondingly, the sequestration flux of SOC (SF-SOC, g·m-2·yr-1) showed an overall increasing trend with average of 82.84 (reed marsh), 151.93 (bare beach) and 123.71 (subtidal flat). Comparing to TOC, the higher MAR had a more distinct effect on carbon sequestration in Liaohe estuarine wetland. The difference in sedimentation rate and carbon sequestration are linked to the changes in sediment flux of riverine input and land utilization in the catchment area due to human activities in recent decades, including the construction of reservoirs, dams and local ditch wharf.

Establishing historical 90Sr activity in seawater of the China seas from 1963 to 2018.

Historical 90Sr activity in seawater was established in the China seas from 1963 to 2018. Based on the exponential decrease in 90Sr activity in seawater, the effective half-life (EHL) of 90Sr was quantified to be 11.5 ± 1.6 a, 16.5 ± 2.4 a, 27.2 ± 6.2 a, and 26.7 ± 4.3 a in the Bohai Sea, Yellow Sea, East China Sea, and South China Sea, respectively. We found contrasting patterns in the EHL of 90Sr and 137Cs in the marginal seas and open oceans that were closely related to the subtly different pathways of 90Sr and 137Cs in marine environment. Additionally, we demonstrated that Fukushima-derived 90Sr (<0.01 Bq/m3) would be difficult to identify in the China seas. Our study not only provided the key parameter of the EHL in marine models for predicting the 90Sr activity in the China seas in the post-Fukushima era but also enhanced our understanding of 90Sr behavior and its fate in marine environments.

Alpha-lipoic acid could attenuate the effect of chemerin-induced diabetic nephropathy progression.

OBJECTIVES: Chemerin is associated with insulin resistance, obesity, and metabolic syndrome. α-lipoic acid (α-LA) is a potent antioxidant involved in the reduction of diabetic symptoms. This study aimed to investigate the relationship between chemerin and P38 MAPK in the progression of diabetic nephropathy (DN) and examine the effects of α-LA on chemerin-treated human mesangial cells (HMCs). MATERIALS AND METHODS: HMCs were transfected with a chemerin-overexpressing plasmid. HMCs were also treated with high-glucose, chemerin, α-LA, PDTC (pyrrolidine dithiocarbamate ammonium, NF-κB p65 inhibitor), and/or SB203580 (P38 MAPK inhibitor). Cell proliferation was tested using the Cell Counting Kit-8 assay. Collagen type IV and laminin were tested by ELISA. Chemerin expression was detected by qRT-PCR. The chemerin receptor was detected by immunohistochemistry. Interleukin-6 (IL-6), tumor necrosis factor-a (TNF-α), nuclear factor-κBp-p65 (NF-κB p-p65), transforming growth factor-ß (TGF-ß), and p-P38 mitogen-activated protein kinase (p-P38 MAPK) were evaluated by western blot. RESULTS: High-glucose culture increased the expression of the chemerin receptor. α-LA inhibited HMC proliferation. Chemerin overexpression increased collagen type IV and laminin expression. P38 MAPK signaling was activated by chemerin, resulting in up-regulation of IL-6, TNF-α, NF-κB p-p65, and TGF-ß. SB203580, PDTC, and α-LA reversed the effects of chemerin, reducing IL-6, TNF-α, NF-κB p-p65, and TGF-ß expression. CONCLUSION: Chemerin might be involved in the occurrence and development of DN. α-LA might prevent the effects of chemerin on the progression of DN, possibly via the P38 MAPK pathway.

Comprehensive evaluation of organophosphate ester contamination in surface water and sediment of the Bohai Sea, China.

This study investigated the occurrence and profile of 14 organophosphate esters (OPEs) in surface water and sediment of the whole Bohai Sea. A total of 53 pairs of surface water and sediment samples were collected and the contained OPEs were quantified using a gas chromatography-mass spectrometry (GC-MS). The average concentrations of OPEs in surface water and sediment were in the range of 0-92.9 ng/L and 0.001-8.58 ng/g dry weight (dw), respectively, with tri (2-chloroethyl) phosphate (TCEP) as the predominant congener in both compartments. The total concentrations of 14 OPEs (∑14OPEs) in surface water and sediment were in the range of 10.9-516.4 ng/L and 1.42-52.9 ng/g dw, respectively. The inventories of ∑14OPEs were calculated to be 179.3 tons in the water and 101.5 tons in the sediment. Based on the risk quotients (RQs), the ecological risks of OPEs to the aquatic organisms in the Bohai Sea were considered to be negligible.

Reduced serum CTRP12 levels in type 2 diabetes are associated with renal dysfunction.

PURPOSE: Serum C1q/TNF-related protein-12 (CTRP12) is one of the newly studied families of adipokines, which is believed to be associated with type 2 diabetes. However, the relationship between serum CTRP12 levels and diabetic nephropathy remains unclear. This study aimed to investigate the relationship between serum CTRP12 levels and renal function in patients with type 2 diabetes. METHODS: A total of 115 type 2 diabetic patients and 54 healthy subjects were enrolled in this study. 52 patients with type 2 diabetes were in the diabetes group (T2DM). The 63 patients with renal dysfunction were diabetic nephropathy group (T2DM-DN) and were divided into microalbuminuria subgroup (31 cases) and macroalbuminuria subgroup (32 cases) according to the 24-h urine protein excretion rate. The concentrations of serum CTRP12 were determined by enzyme-linked immunosorbent assay. RESULTS: Serum CTRP12 level in T2DM and T2DM-DN groups was significantly lower compared with the control group, while CTRP12 level in T2DM-DN group was significantly lower than that in T2DM group, and was associated with the severity of renal insufficiency. After adjusting for gender and age, serum CTRP12 level was negatively correlated with the duration of diabetes, blood urea nitrogen (BUN), uric acid (UA) and 24-h urinary albumin excretion rate (UAE) in T2DM patients. Logistic regression analysis showed that serum CTRP12 level was significantly associated with renal dysfunction in type 2 diabetes mellitus. And the duration of diabetes, total cholesterol (CHOL) and neutrophils/lymphocytes (NLR) are independent risk factors for renal dysfunction in type 2 diabetes mellitus. CONCLUSION: Serum CTRP12 may be involved in the occurrence and development of diabetic nephropathy. Trial registration number and date of registration ChiCTR2000030794, March 14, 2020.