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The La Niña of 2007/2008 was particularly strong, so was the southward flow of the cold, nutrient-rich Changjiang (Yangtze River) Diluted Water (CDW) when the winter monsoon started to blow in the fall. Here we use shipboard data in 2008 in two transects, one in the southwestern East China Sea and one in the southern Taiwan Strait, to show that as late as April in 2008 the CDW was still clearly identifiable when the winter monsoon had weakened. Waters as cold as 16 °C with a salinity lower than 30 still occupied the southwestern East China Sea. Waters of 17 °C and S < 32 could also be found off the coast of China in the central Taiwan Strait. The concentration of NO3 + NO2 was higher than 18 μmol L−1 at both places, which was as much as 40 times higher than the northward moving South China Sea (SCS) water to the east. As a result, the Changjiang River plume may be a significant source of nutrients, particularly N, to the oligotrophic, N-poor SCS, especially in the La Niña years. Indeed, colder and more turbid CDW was more intense and went farther south in 2008 compared with the normal springs of 2006, 2007 and 2009. [ABSTRACT FROM AUTHOR]

Adipose tissue inflammation is closely associated with the development of obesity and insulin resistance. Free fatty acids (FFAs) are a major inducer of obesity-related insulin resistance. Previously, we reported that endoplasmic reticulum (ER) stress potentially mediated retinal inflammation in diabetic retinopathy. The unfolded protein response (UPR) protects cells against damage induced by oxidative stress. X-box binding protein 1 (XBP1) plays a major role in protecting cells by modulating the UPR. However, the link between ER stress and adipocyte inflammation has been poorly investigated. In the present study, we found that pretreatment of 3T3-L1 adipocytes with a low dose of ER stress inducer tunicamycin inhibited FFA-induced upregulated expression of inflammatory cytokines. In addition, FFAs induced phosphorylation of the p65 subunit of NF-κB was largely inhibited by pretreatment with tunicamycin in 3T3-L1 adipocytes. Knockdown of XBP1 by siRNA markedly mitigated the protective effects of preconditioning against inflammation. Conversely, overexpression of XBP1 alleviated FFA-induced phosphorylation of IκB-α, IKKα/β, and NF-κB, which was accompanied by decreased inflammatory cytokine expression. Collectively, these results imply a beneficial role of ER stress preconditioning in protecting against FFA-induced 3T3-L1 adipocyte inflammation, which is likely mediated through inhibition of the IKK/NF-κB pathway via XBP1. [ABSTRACT FROM AUTHOR]

CSNK2B, which encodes the beta subunit of casein kinase II (CK2), plays an important role in neuron morphology and synaptic transmission. Variants in CSNK2B associated with epilepsy and/or intellectual disability (ID)/developmental delay (DD) have been reported in five cases only. Among the 816 probands suspected hereditary epilepsy whose initial report of trio-based whole exome sequencing (WES) were negative, 10 de novo pathogenic or likely pathogenic variants of CSNK2B in nine probands were identified after reanalysis of their raw Trio-WES data. Six of the nine epileptic patients had ID/DD. The age of seizure onset of these nine patients with CSNK2B variants ranged from 2–12 months. Eight patients had age of seizure onset of less than 6 months. The epilepsy of most probands (8/9) was generalized tonic-clonic seizure and clustered (6/9). Most patients had normal electroencephalogram (5/9) and brain magnetic resonance image (7/9) results. Most patients (7/9) had easy-to-control seizures. Levetiracetam was the most commonly used drug in seizure-free patients (5/7). The variants detected in five patients (5/9, 55.6%) were located in the zinc-binding domain. In summary, our research provided evidence that variants in CSNK2B are associated with epilepsy with or without ID/DD. CSNK2B-related epilepsy is relatively easy to be controlled. The zinc-binding domain appears to be the hotspot region for mutation. [ABSTRACT FROM AUTHOR]