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A two-year (2020-2021) survey dataset of six water quality parameters (pH, dissolved oxygen (DO), chemical oxygen demand (COD), dissolved inorganic nitrogen (DIN), soluble reactive phosphate (SRP), and petroleum pollutants) was used to investigate their spatial distribution in the Bohai Sea and quantify their potential sources. There were significant differences in spatial distribution of the parameters. High concentrations of COD, DIN and SRP were found in three bays, with terrestrial input being the main pollution source. Phosphorus-limiting conditions were present in the Bohai Sea. High petroleum pollutant concentrations were identified in port areas, offshore oilfields, and adjacent areas. The pH was above the global oceanic average and there were no signs of acidification. The contribution of the mixed terrestrial inputs, maritime transportation, and offshore oil exploitation sources, oceanic and associated biotic sources, and seawater-atmosphere exchange and atmospheric deposition sources to water quality were 63.4 %, 8.0 %, and 28.6 %, respectively., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

A tide gate was built in 2010 to prevent seawater from moving upstream into the Yongdingxin River estuary in Bohai Bay, Northern China. We analysed the concentrations of Hg, Cd, Pb, TOC, TN, δ 13 C and δ 15 N and studied their variations in the surface layer and vertical profiles of sediment cores collected from the Yongdingxin River estuary. Contamination factors and geo-accumulation indices were calculated for each metal, which revealed high levels of contamination for Hg and Cd in the sediments, likely from anthropogenic sources. δ 13 C and δ 15 N were used as natural tracers to determine the sources of TOC and TN. The results revealed that sewage was the main source of TOC, while TN may have more than one source in the Yongdingxin River estuary. Sewage dominated trace metal pollution in the Yongdingxin River estuary. Our results provide a baseline for trace metal contamination in an estuary facing a large water project., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Focal segmental glomerulosclerosis (FSGS) is a histological lesion with many causes, including inherited genetic defects, with significant proteinuria being the predominant clinical finding at presentation. Mutations in COL4A3 and COL4A4 are known to cause Alport syndrome (AS), thin basement membrane nephropathy, and to result in pathognomonic glomerular basement membrane (GBM) findings. Secondary FSGS is known to develop in classic AS at later stages of the disease. Here, we present seven families with rare or novel variants in COL4A3 or COL4A4 (six with single and one with two heterozygous variants) from a cohort of 70 families with a diagnosis of hereditary FSGS. The predominant clinical finding at diagnosis was proteinuria associated with hematuria. In all seven families, there were individuals with nephrotic-range proteinuria with histologic features of FSGS by light microscopy. In one family, electron microscopy showed thin GBM, but four other families had variable findings inconsistent with classical Alport nephritis. There was no recurrence of disease after kidney transplantation. Families with COL4A3 and COL4A4 variants that segregated with disease represent 10% of our cohort. Thus, COL4A3 and COL4A4 variants should be considered in the interpretation of next-generation sequencing data from such patients. Furthermore, this study illustrates the power of molecular genetic diagnostics in the clarification of renal phenotypes.

Concentrations of heavy metals in river water and sediment were investigated in nine estuaries along the coast of Bohai Bay, Northern China. Multivariate statistical techniques such as principal component analysis and cluster analysis, in combination with metal concentration analysis and correlation analysis, were used to identify the possible sources of the metals and the pollution pattern in nine estuaries along the coast of Bohai Bay. The environmental risks of metals, evaluated by sediment quality guidelines and background values, revealed Hg contamination in the estuaries. However, levels of Cd in estuarine sediments were low, and they were less than those levels in river sediments, partly due to the high mobility and dilution of river or seawater. Cd did not contribute to sediment deposits in estuaries. High organic matter from effluents from large municipal sewage treatment plants was predominantly responsible for restricting Hg mobility from the river to Bohai Bay., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

The polysaccharides extracted by hot water and precipitated by 50% ethanol from the fruiting bodies of cultured Cordyceps militaris (W-CBP50) were introduced. Antioxidant activities of W-CBP50, W-CBP50 I (obtained from W-CBP50 purified by Sephadex G-100 chromatography) and W-CBP50 II (obtained from W-CBP50I purified by Sephadex G-200 chromatography) were evaluated and structural features of W-CBP50 II were analyzed. The polysaccharide W-CBP50 II was able to scavenge the stable free radical 1,1-diphenyl-2-picrylhyrazyl (DPPH), while W-CBP50 and W-CBP50I could scavenge DPPH, hydroxyl and superoxide radical. Structural characteristics of W-CBP50 II were investigated using GPC, GC-MS, (1)H NMR and IR. The results showed that it was mainly composed of α-glucose, α-mannose, α-galactose and α-arabinose with α-type glycosidic linkage and the molecular weight of its main component was 8.97 kD., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Focal and segmental glomerulosclerosis (FSGS) is a major cause of end-stage kidney disease. Recent advances in molecular genetics show that defects in the podocyte play a major role in its pathogenesis and mutations in inverted formin 2 (INF2) cause autosomal dominant FSGS. In order to delineate the role of INF2 mutations in familial and sporadic FSGS, we sought to identify variants in a large cohort of patients with FSGS. A secondary objective was to define an approach for genetic screening in families with autosomal dominant disease. A total of 248 individuals were identified with FSGS, of whom 31 had idiopathic disease. The remaining patients clustered into 64 families encompassing 15 from autosomal recessive and 49 from autosomal dominant kindreds. There were missense mutations in 8 of the 49 families with autosomal dominant disease. Three of the detected variants were novel and all mutations were confined to exon 4 of INF2, a regulatory region responsible for 90% of all changes reported in FSGS due to INF2 mutations. Thus, in our series, INF2 mutations were responsible for 16% of all cases of autosomal dominant FSGS, with these mutations clustered in exon 4. Hence, screening for these mutations may represent a rapid, non-invasive and cost-effective method for the diagnosis of autosomal dominant FSGS.

The pharmacokinetics of enrofloxacin and its active metabolite ciprofloxacin were investigated in the Chinese mitten-handed crab after a single intramuscular injection of enrofloxacin at 5.0mg/kg body weight. The tissue concentrations of enrofloxacin and ciprofloxacin were determined simultaneously by a high-performance liquid chromatography (HPLC) method. The data were analyzed with Practical Pharmacokinetic Program 3P97. The highest average concentrations of enrofloxacin in liver, muscle, gill, and hemolymph were 3.93, 12.42, 16.73, and 11.04 microg/g (ml), respectively. The elimination half-lives (t(1/2beta)) for enrofloxacin were 92.42, 64.86, 38.80, and 52.39 h, respectively. The AUC(0-infinity) values for enrofloxacin were 304.80, 260.74, 288.30, and 269.24 microg h/ml, respectively. Ciprofloxacin could be detected in all four tissues. The respective values of main pharmacokinetics parameters Cmax, t(1/2beta), and AUC(0-infinity) were 0.52 microg/g (ml), 38.38 h, and 35.06 microg h/ml for liver; 0.24 microg/g (ml), 65.36 h, and 25.64 microg h/ml for muscle; 0.10 microg/g (ml), 112.88 h, and 11.57 microg h/ml for gill; and 0.30 microg/g (ml), 93.33 h, and 39.99 microg h/ml for hemolymph.

Huntington's disease results from expansion of the polyglutamine (PolyQ) domain in the huntingtin protein. Although the cellular mechanism by which pathologic-length PolyQ protein causes neurodegeneration is unclear, mitochondria appear central in pathogenesis. We demonstrate in isolated mitochondria that pathologic-length PolyQ protein directly inhibits ADP-dependent (state 3) mitochondrial respiration. Inhibition of mitochondrial respiration by PolyQ protein is not due to reduction in the activities of electron transport chain complexes, mitochondrial ATP synthase, or the adenine nucleotide translocase. We show that pathologic-length PolyQ protein increases the production of reactive oxygen species in isolated mitochondria. Impairment of state 3 mitochondrial respiration by PolyQ protein is reversed by addition of the antioxidants N-acetyl-L-cysteine or cytochrome c. We propose a model in which pathologic-length PolyQ protein directly inhibits mitochondrial function by inducing oxidative stress.