北部湾鱼类碳、氮、磷生态化学计量特征

为探究北部湾鱼类生态化学计量特征,于2021年3月—4月采集分析了北部湾沿岸9个渔港的79种鱼类(382尾)碳(C)、氮(N)、磷(P)含量特征。结果表明北部湾鱼类C、N、P元素含量变化范围分别为33.87%—58.34%、6.31%—14.92%和0.77%—4.67%;C∶N、C∶P、N∶P的变化范围分别为3.43—9.72、19.15—173.06和5.04—33.68,其中P元素含量变化最大,导致C∶P和N∶P的变化。不同物种在科间的差异较大,科内的差异较小。不同体型和食性鱼类之间的C、N、P含量及比值具有显著差异(P<0.05)。鱼类的C∶P和N∶P与P含量呈显著负相关(R²=0.966,P<0.01;R²=0.877,P<0.01),P含量和Ca含量呈显著正相关(R²=0.919,P<0.01),P含量的变化可能与鱼类骨骼和鳞片的形成有关。总之,北部湾鱼类未保持严格的生态化学计量平衡,鱼类生态化学计量特征存在显著的种间差异,主要因鱼类不同的体型和食性差异所致。     

Chromosomal deletions and inversions mediated by TALENs and CRISPR/Cas in zebrafish

Customized TALENs and Cas9/gRNAs have been used for targeted mutagenesis in zebrafish to induce indels into protein-coding genes. However, indels are usually not sufficient to disrupt the function of non-coding genes, gene clusters or regulatory sequences, whereas large genomic deletions or inversions are more desirable for this purpose. By injecting two pairs of TALEN mRNAs or two gRNAs together with Cas9 mRNA targeting distal DNA sites of the same chromosome, we obtained predictable genomic deletions or inversions with sizes ranging from several hundred bases to nearly 1 Mb. We have successfully achieved this type of modifications for 11 chromosomal loci by TALENs and 2 by Cas9/gRNAs with different combinations of gRNA pairs, including clusters of miRNA and protein-coding genes. Seven of eight TALEN-targeted lines transmitted the deletions and one transmitted the inversion through germ line. Our findings indicate that both TALENs and Cas9/gRNAs can be used as an efficient tool to engineer genomes to achieve large deletions or inversions, including fragments covering multiple genes and non-coding sequences. To facilitate the analyses and application of existing ZFN, TALEN and CRISPR/Cas data, we have updated our EENdb database to provide a chromosomal view of all reported engineered endonucleases targeting human and zebrafish genomes.     

Transactivation of Atg4b by C/EBPβ Promotes Autophagy To Facilitate Adipogenesis

Autophagy is a highly conserved self-digestion pathway involved in various physiological and pathophysiological processes. Recent studies have implicated a pivotal role of autophagy in adipocyte differentiation, but the molecular mechanism for its role and how it is regulated during this process are not clear. Here, we show that CCAAT /enhancer-binding protein β (C/EBPβ), an important adipogenic factor, is required for the activation of autophagy during 3T3-L1 adipocyte differentiation. An autophagy-related gene, Atg4b, is identified as a de novo target gene of C/EBPβ and is shown to play an important role in 3T3-L1 adipocyte differentiation. Furthermore, autophagy is required for the degradation of Klf2 and Klf3, two negative regulators of adipocyte differentiation, which is mediated by the adaptor protein p62/SQSTM1. Importantly, the regulation of autophagy by C/EBPβ and the role of autophagy in Klf2/3 degradation and in adipogenesis are further confirmed in mouse models. Our data describe a novel function of C/EBPβ in regulating autophagy and reveal the mechanism of autophagy during adipocyte differentiation. These new insights into the molecular mechanism of adipose tissue development provide a functional pathway with therapeutic potential against obesity and its related metabolic disorders.     

正常大鼠胃黏膜中肌球蛋白轻链激酶定性和定位观察

目的观察正常大鼠胃组织中肌球蛋白轻链激酶的表达及分布特点。方法取11只SD正常雄性大鼠,在饥饿状态下,处死后取胃组织。通过免疫组化染色,观察正常大鼠胃组织中MLCK的表达及分布。结果MLCK在黏膜肌层、肌层和黏膜下层血管壁平滑肌均有大量表达;在胃底腺中,MLCK主要表达于壁细胞和主细胞胞浆内。结论MLCK不仅存在于平滑肌细胞内,还分布于胃底腺壁细胞和主细胞内,可能参与胃底腺腺细胞的分泌活动。     

Hic‐5 deficiency protects cerulein‐induced chronic pancreatitis via down‐regulation of the NF‐κB (p65)/IL‐6 signalling pathway

Chronic pancreatitis (CP), characterized by pancreatic fibrosis, is a recurrent, progressive and irreversible disease. Activation of the pancreatic stellate cells (PSCs) is considered a core event in pancreatic fibrosis. In this study, we investigated the role of hydrogen peroxide‐inducible clone‐5 (Hic‐5) in CP. Analysis of the human pancreatic tissue samples revealed that Hic‐5 was overexpressed in patients with CP and was extremely low in healthy pancreas. Hic‐5 was significant up‐regulated in the activated primary PSCs independently from transforming growth factor beta stimulation. CP induced by cerulein injection was ameliorated in Hic‐5 knockout (KO) mice, as shown by staining of tissue level. Simultaneously, the activation ability of the primary PSCs from Hic‐5 KO mice was significantly attenuated. We also found that the Hic‐5 up‐regulation by cerulein activated the NF‐κB (p65)/IL‐6 signalling pathway and regulated the downstream extracellular matrix (ECM) genes such as α‐SMA and Col1a1. Therefore, we determined whether suppressing NF‐κB/p65 alleviated CP by treating mice with the NF‐κB/p65 inhibitor triptolide in the cerulein‐induced CP model and found that pancreatic fibrosis was alleviated by NF‐κB/p65 inhibition. These findings provide evidence for Hic‐5 as a therapeutic target that plays a crucial role in regulating PSCs activation and pancreatic fibrosis.     

Tle1 attenuates hepatic ischemia/reperfusion injury by suppressing NOD2/NF-κB signaling

ABSTRACT

Liver damage induced by ischemia/reperfusion (I/R) remains a primary issue in multiple hepatic surgeries. Innate immune-mediated inflammatory responses during the reperfusion stage aggravate the injury. Nevertheless, the detailed mechanism of hepatic I/R has not been fully clarified yet. Our research focuses on the role of Transducin-like enhancer of split-1 (Tle1) in the liver I/R injury and the relation between Tle1 and Nucleotide-binding oligomerization domain 2 (NOD2). To answer these questions, we constructed mouse models of I/R and cell models of hypoxia/reoxygenation (H/R). We found decreased Tle1 accompanied by increased NOD2 during reperfusion. Mice pro-injected with Tle1-siRNA emerged aggravated liver dysfunction. Repression of Tle1 had a significant impact on NOD2 and downstream NF-κB signaling in vitro. However, alteration of NOD2 failed to affect the expression of Tle1. To conclude, our study demonstrates that Tle1 shelters the liver from I/R injury through suppression of NOD2-dependent NF-κB activation and subsequent inflammatory responses.     

Notch inhibition promotes fetal liver stem/progenitor cells differentiation into hepatocytes via the inhibition of HNF-1β

In a previous study, the Notch pathway inhibited with N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (also called DAPT) was shown to promote the differentiation of fetal liver stem/progenitor cells (FLSPCs) into hepatocytes and to impair cholangiocyte differentiation. The precise mechanism for this, however, was not elucidated. Two mechanisms are possible: Notch inhibition might directly up-regulate hepatocyte differentiation via HGF (hepatocyte growth factor) and HNF (hepatocyte nuclear factor)-4α or might impair cholangiocyte differentiation thereby indirectly rendering hepatocyte differentiation as the dominant state. In this study, HGF and HNF expression was detected after the Notch pathway was inhibited. Although our initial investigation indicated that the inhibition of Notch induced hepatocyte differentiation with an efficiency similar to the induction via HGF, the results of this study demonstrate that Notch inhibition does not induce significant up-regulation of HGF or HNF-4α in FLSPCs. This suggests that Notch inhibition induces hepatocyte differentiation without the influence of HGF or HNF-4α. Moreover, significant down-regulation of HNF-1β was observed, presumably dependent on an impairment of cholangiocyte differentiation. To confirm this presumption, HNF-1β was blocked in FLSPCs and was followed by hepatocyte differentiation. The expression of markers of mature cholangiocyte was impaired and hepatocyte markers were elevated significantly. The data thus demonstrate that the inhibition of cholangiocyte differentiation spontaneously induces hepatocyte differentiation and further suggest that hepatocyte differentiation from FLSPCs occurs at the expense of the impairment of cholangiocyte differentiation, probably being enhanced partially via HNF-1β down-regulation or Notch inhibition.     

1982-2012年中亚地区植被时空变化特征及其与气候变化的相关分析

干旱区植被生态系统对气候变化极为敏感,并且干旱区的植被变化研究对全球碳循环具有重要意义。然而近几十年来,中亚干旱区植被对气候变化的响应机制尚不甚明朗。利用归一化植被指数NDVI数据集和MERRA（Modern-Era Retrospective Analysis for Research and Applications）气象数据,采用经验正交函数（EOF,Empirical Orthogonal Function）和最小二乘法等方法系统分析了31a（1982-2012年）来中亚地区NDVI在不同时间尺度的时空变化特征。进一步分析和研究NDVI与气温和降水的相关性,结果表明：1982-2012年,中亚地区年NDVI总体呈现缓慢增长趋势,而1994年以后年NDVI呈现明显下降趋势,尤其在哈萨克斯坦北部草原地区下降趋势尤为突出。这可能是由于过去30年间,中亚地区降水累计量的持续减少造成的。NDVI的季节变化表明春季NDVI增长最为明显,冬季则显著下降。与平原区相比,中亚山区的NDVI值增长幅度最大,并且山区年NDVI与季节NDVI呈现显著增加趋势（P < 0.05）。中亚地区年NDVI与年降水量正相关,而年NDVI与气温变化存在弱负相关。年NDVI和气温的正相关中心在中亚南部地区,负相关中心则出现在哈萨克斯坦的西部和北部地区;NDVI和降水的相关性中心刚好与气温相反。此外,在近30年间的每年6月至9月,中亚地区NDVI与气温存在近一个月的时间延迟现象。本研究为中亚干旱区生态系统变化和中亚地区碳循环的估算提供科学依据。