Toward Quantifying the Increasing Accessibility of the Arctic Northeast Passage in the Past Four Decades

Sea ice,one of the most dominant barriers to Arctic shipping,has decreased dramatically over the past four decades.Arctic maritime transport is hereupon growing in recent years.To produce a long-term assessment of trans-Arctic accessibility,we systematically revisit the daily Arctic navigability with a view to the combined effects of sea ice thickness and concentration throughout the period 1979−2020.The general trends of Navigable Windows(NW)in the Northeast Passage show that the number of navigable days is steadily growing and reached 89±16 days for Open Water(OW)ships and 163±19 days for Polar Class 6(PC6)ships in the 2010s,despite high interannual and interdecadal variability in the NWs.More consecutive NWs have emerged annually for both OW ships and PC6 ships since 2005 because of the faster sea ice retreat.Since the 1980s,the number of simulated Arctic routes has continuously increased,and optimal navigability exists in these years of record-low sea ice extent(e.g.,2012 and 2020).Summertime navigability in the East Siberian and Laptev Seas,on the other hand,varies dramatically due to changing sea ice conditions.This systematic assessment of Arctic navigability provides a reference for better projecting the future trans-Arctic shipping routes.

Cell polarity protein Par3 complexes with DNA-PK via Ku70 and regulates DNA double-strand break repair

分区有缺陷者 3 (Par3 ) ，在 conservedPar3/Par6/aPKC 建筑群的一个关键部件，在房间极性的戏基础角色。此处，我们报导 Ku70 和通过试管内绑定试金的蛋白质由液体层析双人脚踏车质谱法跟随了的 Ku80 同样新奇的交往 Par3 的鉴定。Ku70/Ku80 蛋白质是 DNA 依赖的蛋白激酶(DNA-PK ) 的二个关键规章的子单元，它在修理双海滨脱氧核糖核酸裂缝(DSB ) 起一个必要作用。我们决定 Par3 withKu70/Ku80 的原子协会被 y 照耀(红外) 提高，有势力 DSB inducer。而且， DNA-PKcs， DNA-PK 的催化子单元，响应红外与 Par3/Ku70/Ku80 建筑群交往了。Par3over 表示或击倒分别地能够 up- 或 downregulat-ing DNA-PK 活动。而且， Par3 击倒的房间被发现在随机的原生质标志集成有缺点，在 DSB 修理追随者红外有缺点、对射线敏感，类似于 Ku70knockdown 房间的显型。这些调查结果作为 DNA-PK 建筑群的一个新奇部件识别 Par3 并且含有到 DSB 修理的房间极性的一个意外连接。

Cell polarity protein Par3 complexes with DNA-PK via Ku70 and regulates DNA double-strand break repair

The author affiliations were mixed up in the previous published version. The third fund number of National NaturalScience Foundation of China in the Acknowledgments was wrong, it should be "30270335". The Shanghai MunicipalCouncil for Science and Technology (No.06DZ22032) was missed in the Acknowledgments. There are some labelingand production errors in Figure 2A, Figure 3B and 3C, Figure 5C, Figure 6B and 6E, Figure 7B and 7D. In Figure 2A,left panel "A431" should be "Par3". In Figure 3B and 3C, "anti-Par3CT" should be "anti-Par3LCT", "GST-Par3CT"should be "GST-Par3LCT". In Figure 5C, the second arrow indicating "Lamin B" should be "[3-tubulin". In Figure 6Bright panel, the molecular weight for ?-actin should be "43" instead of"200". In Figure 6E, "Par3" should be "Par3i". Themolecular weight for the DNA-PKcs panel should be the same as the p-DNA-PKcs. In Figure 7B, the time point "240"in the left panel should be "120"; in the right panel of Figure 7B, the title for the y axis should be "DNA released (%)".In Figure 7D, the title for the y axis should be "Survival (%)", and the scale for the y axis should be "100, 10 and 1". These corrections do not affect the conclusions of the study. We apologize for any inconvenience this may havecaused.

MFSD12 affects glycosphingolipid metabolism by modulating lysosome homeostasis

Dear Editor,Glycosphingolipid(GSL)catabolism is strictly regulated in a sequential manner by lysosomal hydrolases with the help of lipid-binding proteins.Impairments of the catabolic pathway cause the onset of lysosomal storage diseases(LsDs),which are characterized by the aberrant accumulation of GSLs(Hannun and Obeid 2018;Breiden and Sandhoff 2019).The primary LSDs occur through the well-known mechanism of inherited defects in genes encoding the catabolic enzymes(or their related cofactors)which reside in the lumen of lysosomes(Hannun and Obeid 2018;Breiden and Sandhoff 2019).However,in some LSDs,the inherited mutations affect other proteins,such as those residing in the lysosomal membrane;these mutations are associated with defects in traffcking and fusion in the endocytic system(Platt et al.2012).However,the non-lumenal lysosomal membrane proteins involved in GSL metabolism remain to be identified.

Regulation of glucose and lipid metabolism in health and disease

Glucose and fatty acids are the major sources of energy for human body. Cholesterol, the most abundant sterol in mammals, is a key component of cell membranes although it does not generate ATP. The metabolisms of glucose, fatty acids and cholesterol are often intertwined and regulated. For example, glucose can be converted to fatty acids and cholesterol through de novo lipid biosynthesis pathways. Excessive lipids are secreted in lipoproteins or stored in lipid droplets. The metabolites of glucose and lipids are dynamically transported intercellularly and intracellularly, and then converted to other molecules in specific compartments. The disorders of glucose and lipid metabolism result in severe diseases including cardiovascular disease, diabetes and fatty liver. This review summarizes the major metabolic aspects of glucose and lipid, and their regulations in the context of physiology and diseases.

PKM2 coordinates glycolysis with mitochondrial fusion and oxidative phosphorylation

A change in the metabolic flux of glucose from mitochondrial oxidative phosphorylation (OXPHOS) to aerobic glycolysis is regarded as one hallmark of cancer. However, the mechanisms underlying the metabolic switch between aerobic glycolysis and OXPHOS are unclear. Here we show that the M2 isoform of pyruvate kinase (PKM2), one of the rate-limiting enzymes in glycolysis, interacts with mitofusin 2 (MFN2), a key regulator of mitochondrial fusion, to promote mitochondrial fusion and OXPHOS, and attenuate glycolysis. mTOR increases the PKM2:MFN2 interaction by phosphorylating MFN2 and thereby modulates the effect of PKM2: MFN2 on glycolysis, mitochondrial fusion and OXPHOS. Thus, an mTOR-MFN2-PKM2 signaling axis couples glycolysis and OXPHOS to modulate cancer cell growth.

mTORC1 signaling in hepatic lipid metabolism

表明小径的 rapamycin (mTOR ) 的机械学的目标在不同机关或纸巾调整许多新陈代谢、生理的过程。mTOR 发信号的 Dysregulation 包括肥胖，糖尿病，癌症，脂肪肝疾病，和 neuronal 在许多人的疾病被含有混乱。这里，我们在理解发信号的 mTORC1 (mTOR 建筑群 1 ) 怎么在肝调整类脂化合物新陈代谢考察最近的进步。

CRTC2 modulates hepatic SREBPlc cleavage by controlling Insig2a expression during fasting

Dear Editor, Dysregulation of hepatic lipid and glucose production results in obesity, diabetes and nonalcoholic fatty liver disease. De novo lipogenesis and gluconeogenesis in the liver con- tribute, at least in part, to the dynamic homeostasis of lipid and glucose levels （Rui, 2014; Han and Wang, 2017）. These processes are regulated at the transcriptional level by dif- ferent transcription factors Jn response to various environ- mental cues, including hormones, nutrition and stress. Regulators of lipogenesis include the sterol regulatory ele- ment-binding proteins （SREBPs）, which are members of the basic helix-loop-helix leucine zipper transcription factor family （Goldstein et al., 2006）. There are three closely rela- ted SREBPs, SREBPla, SREBPlc and SREBP2, among which SREBPlc and SREBP2 are the major isoforms expressed in the liver. SREBPlc mainly regulates fatty acid synthesis.

Evaluation indexes for symptom changes in Chinese medicine

OBJECTIVE: To screen and summarize evaluation indexes for symptom changes in Chinese medicine(CM).METHODS: A case database was established based on information from subsequent patient visits from the case records of famous doctors since 1866.Symptom change descriptions in the database were regarded as research materials. The evaluation indexes of the symptom changes were screened and summarized.RESULTS: In total, 243 evaluation indexes for 256symptoms were summarized. Among them, common symptoms were frequency, quantity, degree,mobility, color, and correlation with fatigue.CONCLUSION: There are many aspects to evaluating the changes in a symptom. Some symptoms occur with other simultaneous symptoms. The alleviation or aggravation of simultaneous symptoms could reflect the corresponding changes in a symptom. The changes of inducing factors are important to judging changes in symptoms.