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Statement on Publication Ethics for Editors and Publishers
Armen Yuri Gasparyan,Marlen Yessirkepov,Alexander A. Voronov,Sergey V. Gorin,Anna M. Koroleva,George D. Kitas 대한의학회 2016 Journal of Korean medical science Vol.31 No.9
The digitization and related developments in journal editing and publishing necessitate increasing the awareness of all stakeholders of science communication in the emerging global problems and possible solutions. Journal editors and publishers are frequently encountered with the fast-growing problems of authorship, conflicts of interest, peer review, research misconduct, unethical citations, and inappropriate journal impact metrics. While the number of erroneous and unethical research papers and wasteful, or ‘predatory’, journals is increasing exponentially, responsible editors are urged to ‘clean’ the literature by correcting or retracting related articles. Indexers are advised to implement measures for accepting truly influential and ethical journals and delisting sources with predatory publishing practices. Updating knowledge and skills of authors, editors and publishers, developing and endorsing recommendations of global editorial associations, and (re) drafting journal instructions can be viewed as potential tools for improving ethics of academic journals. The aim of this Statement is to increase awareness of all stakeholders of science communication of the emerging ethical issues in journal editing and publishing and initiate a campaign of upgrading and enforcing related journal instructions.
Cholesterol modulates ion channels via down-regulation of phosphatidylinositol 4,5-bisphosphate
Chun, Yoon Sun,Shin, Sora,Kim, Yonjung,Cho, Hana,Park, Myoung Kyu,Kim, Tae-Wan,Voronov, Sergey V.,Di Paolo, Gilbert,Suh, Byung-Chang,Chung, Sungkwon Blackwell Publishing Ltd 2010 Journal of Neurochemistry Vol.112 No.5
<P><I>J. Neurochem.</I> (2010) <B>112</B>, 1286–1294.</P><P>Abstract</P><P>Ubiquitously expressed Mg<SUP>2+</SUP>-inhibitory cation (MIC) channels are permeable to Ca<SUP>2+</SUP> and Mg<SUP>2+</SUP> and are essential for cell viability. When membrane cholesterol level was increased by pre-incubating cells with a water-soluble form of cholesterol, the endogenous MIC current in HEK293 cells was negatively regulated. The application of phosphatidylinositol 4,5-bisphosphate (PIP<SUB>2</SUB>) recovered MIC current from cholesterol effect. As PIP<SUB>2</SUB> is the direct modulator for MIC channels, high cholesterol content may cause down-regulation of PIP<SUB>2</SUB>. To test this possibility, we examined the effect of cholesterol on two exogenously expressed PIP<SUB>2</SUB>-sensitive K<SUP>+</SUP> channels: human <I>Ether-a-go-go</I> related gene (HERG) and KCNQ. Enrichment with cholesterol inhibited HERG currents, while inclusion of PIP<SUB>2</SUB> in the pipette solution blocked the cholesterol effect. KCNQ channel was also inhibited by cholesterol. The effects of cholesterol on these channels were blocked by pre-incubating cells with inhibitors for phospholipase C, which may indicate that cholesterol enrichment induces the depletion of PIP<SUB>2</SUB> via phospholipase C activation. Lipid analysis showed that cholesterol enrichment reduced &ggr;-<SUP>32</SUP>P incorporation into PIP<SUB>2</SUB> by approximately 35%. Our results suggest that cholesterol may modulate ion channels by changing the levels of PIP<SUB>2</SUB>. Thus, an important cross-talk exists among two plasma membrane-enriched lipids, cholesterol and PIP<SUB>2</SUB>.</P>